Podcasts about neurotransmission

Welcome all to IS PHARMACOLOGY DIFFICULT Podcast! I am Dr Radhika VijayIn this episode, I will be giving an talking about the Chemical Neurotransmission in the CNS. It will involve the different steps in Neurotransmission like synthesis, storage, release, effect etc.I will also give some details about Fast and Slow Neurotransmission and different examples for each of these. Looking forward to a great and long 4th season of the podcast which would definitely turn out to be more knowledgeable and interesting!!For all the updates and latest episodes of my podcast, please visit www.ispharmacologydifficult.com where you can also sign up for a free monthly newsletter of mine."Pharmacology Further" E-Newsletter and Podcast:The links for these are at all my websites and specifically:Link for E-Newsletter: https://pharmacologyfurther.substack.com/Link for the E-Newsletter Podcast: https://www.pharmacologyfurther.comIt actually contains lot of updates about the medical sciences, drug information and my podcast updates also.You can follow me on different social media handles like twitter, insta, facebook and linkedin. They all are with same name "IS PHARMACOLOGY DIFFICULT". If you are listening for the first time, do follow me here, whatever platform you are consuming this episode, stay tuned, do rate and review on ITunes, Apple podcasts, stay safe, stay happy, stay enlightened, Thank you!! Please leave Review on Apple podcasts! My E-Newsletter sign up at Substack! Connect on Twitter & Instagram! My books on Amazon & Goodreads!

Welcome all to IS PHARMACOLOGY DIFFICULT Podcast! I am Dr Radhika VijayIn this episode, I will be giving an talking about the Chemical Neurotransmission in the CNS. It will involve the different steps in Neurotransmission like synthesis, storage, release, effect etc.I will also give some details about Fast and Slow Neurotransmission and different examples for each of these.Looking forward to a great and long 4th season of the podcast which would definitely turn out to be more knowledgeable and interesting!!For all the updates and latest episodes of my podcast, please visit www.ispharmacologydifficult.com where you can also sign up for a free monthly newsletter of mine."Pharmacology Further" E-Newsletter and Podcast:The links for these are at all my websites and specifically:Link for E-Newsletter: https://pharmacologyfurther.substack.com/Link for the E-Newsletter Podcast: https://www.pharmacologyfurther.comIt actually contains lot of updates about the medical sciences, drug information and my podcast updates also.You can follow me on different social media handles like twitter, insta, facebook and linkedin. They all are with same name "IS PHARMACOLOGY DIFFICULT". If you are listening for the first time, do follow me here, whatever platform you are consuming this episode, stay tuned, do rate and review on ITunes, Apple podcasts, stay safe, stay happy, stay enlightened, Thank you!!Please leave Review on Apple podcasts!My E-Newsletter sign up at Substack!Connect on Twitter & Instagram!My books on Amazon & Goodreads!

Join us as we cover a set of papers published in November 2023 on treatments targeting cholinergic transmission in Alzheimer's disease. In this episode hosted by Christy, we will go over various topics, from drug discovery using synthesized compounds to drug testing of plant extracts, as well as improving drug delivery through the blood-brain barrier. Enjoy! Papers evaluating synthesized compounds (2:00)  Papers targeting AchE (10:45)-------------------------------------------------------------- You can find the bibliography for this episode here, or by clicking the link below:https://drive.google.com/file/d/1wh1EFtB3KrW0J6CHd_i-NxOaSZxZdXyT/view?usp=drive_linkTo access the folder with ALL our bibliographies, follow this link (it will be updated as we publish episodes and process bibliographies), or use the link below:https://drive.google.com/drive/folders/1bzSzkY9ZHzzY8Xhzt0HZfZhRG1Gq_Si-?usp=sharingYou can also find all of our bibliographies on our website: amindr.com. -------------------------------------------------------------- Follow-up on social media for more updates!Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastFacebook:  AMiNDR  Youtube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us spread the word about AMiNDR to your friends, colleagues, and networks! And if you could leave us a rating and/or review on your streaming app of choice (Apple Podcasts, Spotify, or wherever you listen to the podcast), that would be greatly appreciated! It helps us a lot and we thank you in advance for leaving a review! Don't forget to subscribe to hear about new episodes as they come out too. Thank you to our sponsor, the Canadian Consortium of Neurodegeneration in Aging, or CCNA, for their financial support of this podcast. This helps us to stay on the air and bring you high quality episodes. You can find out more about the CCNA on their website: https://ccna-ccnv.ca/. Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted and hosted by Christy Yu, edited by Isabelle Vaux, and reviewed by Anusha Kamesh. The bibliography was made by Rob Cloke and wordcloud was created by Salodin Al-Achkar (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For November 2023, the sorters were Elyn Rowe, Christy Yu, Salodin Al-Achkar, Naila Kuhlmann and Anusha Kamesh. Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, Lara Onbasi, Joseph Liang, Judy Cheng, and Christy Yu, for keeping everything running smoothly. AMiNDR was founded in 2020 by Sarah Louadi, Ellen Koch, Elyn Rowe, and Naila Kuhlmann. Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

Here are 8 simple, practical ways to beat brain fog that you can start today.  Brain fog is the frustrating experience of cloudy, slowed thinking. Many of us have experienced it at some point, but if you're struggling with it regularly, there's a lot that you can do. Tune in!  And if you have any additional questions you would like answered in the future, let me know in the comments!   Watch/Read Next… How to Get Rid of Brain Fog: Your Action Plan: https://drruscio.com/how-to-get-rid-of-brain-fog/  Brain Fog: A Research-Based Guide to Restoring Mental Clarity: https://drruscio.com/brain_fog/  Iron Deficiency Basics: https://drruscio.com/can-low-iron-cause-digestive-issues/  Vitamin B12 Deficiency More Common Than Thought: https://drruscio.com/vitamin-b12-deficiency-more-common-than-thought/  How to Boost Your Health with High Protein Snacks: https://drruscio.com/high-protein-snacks/  Chronic Fatigue with Dr. Jenny Tufenkian: https://drruscio.com/chronic-fatigue-and-viruses/    Timestamps 00:00 Intro  03:35 Iron  06:28 Vitamin B12  08:38 Probiotics  13:14 Hormones  15:54 Sleep  19:27 Acetyl-l-carnitine  22:40 Exercise  26:31 Protein  29:07 Forest bathing  32:15 A great brain fog diet 34:16 The role of chronic infections    Featured Studies  Understanding the Experience and Impacts of Brain Fog in Chronic Pain: https://pubmed.ncbi.nlm.nih.gov/37441085/  How nature nurtures: Amygdala activity decreases as the result of a one-hour walk in nature: https://pubmed.ncbi.nlm.nih.gov/36059042/  Associations between Nature Exposure and Health: https://pubmed.ncbi.nlm.nih.gov/33946197/  Spending at least 120 minutes a week in nature is associated with good health and wellbeing: https://pubmed.ncbi.nlm.nih.gov/31197192/  Sleep drives metabolite clearance from the adult brain: https://pubmed.ncbi.nlm.nih.gov/24136970/  Poorer sleep impairs brain health at midlife: https://pubmed.ncbi.nlm.nih.gov/36725955/  Resetting the late timing of 'night owls' has a positive impact on mental health and performance: https://pubmed.ncbi.nlm.nih.gov/31202686/  Exercise training increases size of hippocampus and improves memory: https://pubmed.ncbi.nlm.nih.gov/21282661/   Effectiveness of physical activity interventions for improving depression, anxiety and distress: https://pubmed.ncbi.nlm.nih.gov/36796860/   The Role of Amino Acids in Neurotransmission and Fluorescent Tools for Their Detection: https://pubmed.ncbi.nlm.nih.gov/32867295/  Long-term dietary protein intake and subjective cognitive decline in US men and women: https://pubmed.ncbi.nlm.nih.gov/34293099/  The misogyny of iron deficiency: https://pubmed.ncbi.nlm.nih.gov/33682094/  Iron treatment normalizes cognitive functioning in young women: https://pubmed.ncbi.nlm.nih.gov/17344500/  How can I get enough iron?: https://www.ncbi.nlm.nih.gov/books/NBK279618/  B Vitamins in the nervous system: Current knowledge of the biochemical modes of action and synergies of thiamine, pyridoxine, and cobalamin: https://pubmed.ncbi.nlm.nih.gov/31490017/  Low Vitamin B12 Levels: An Underestimated Cause Of Minimal Cognitive Impairment And Dementia: https://pubmed.ncbi.nlm.nih.gov/32206454/ Vitamin B12 - Health Professional Fact Sheet: https://ods.od.nih.gov/factsheets/VitaminB12-HealthProfessional/#h3  A Paleolithic Diet with and without Combined Aerobic and Resistance Exercise Increases Functional Brain Responses and Hippocampal Volume in Subjects with Type 2 Diabetes: https://pubmed.ncbi.nlm.nih.gov/29255413/  Hormonal Influences on Cognitive Function: https://pubmed.ncbi.nlm.nih.gov/30914845/  Effect of standardized root extract of ashwagandha ( Withania somnifera) on well-being and sexual performance in adult males: https://pubmed.ncbi.nlm.nih.gov/35873404/  Benefits of Black Cohosh (Cimicifuga racemosa) for Women Health: https://pubmed.ncbi.nlm.nih.gov/35337076/ Probiotics fortify intestinal barrier function: https://pubmed.ncbi.nlm.nih.gov/37168869/  Probiotic supplementation improved cognitive function in cognitively impaired and healthy older adults: https://pubmed.ncbi.nlm.nih.gov/36529793/     Get the Latest Updates Facebook - https://www.facebook.com/DrRusciodc Instagram - https://www.instagram.com/drrusciodc/ Pinterest - https://www.pinterest.com/drmichaelrusciodc    DISCLAIMER: The information on this site is not intended or implied to be a substitute for professional medical advice, diagnosis or treatment. Always seek the advice of your physician or other qualified healthcare provider before starting any new treatment or discontinuing an existing treatment. Music featured in this video: "Modern Technology" by Andrew G, https://audiojungle.net/user/andrew_g  *Full transcript available on YouTube by clicking the “Show transcript” button on the bottom right of the video.

I am thrilled to have Dr. Ana Andreazza, a distinguished professor at the University of Toronto, where she holds esteemed positions within the departments of Pharmacology and Toxicology, as well as Psychiatry. As the holder of a prestigious Canada Research Chair in Molecular Pharmacology of Mood Disorders, Dr. Andreazza's expertise delves into the intricate interplay between molecular pharmacology and mental health.At the forefront of groundbreaking research, Dr. Andreazza wears another significant hat as the Scientific Director of the Mitochondrial Innovation Initiative (Mito2i). Her remarkable contributions extend to the publication of over 150 research articles, garnering an impressive 9,000 citations. Dr. Andreazza's exceptional influence in the realm of mitochondrial research is particularly notable in its application to mental health, specifically mood disorders.Through her unwavering commitment to unraveling the mysteries of mitochondria and their profound impact on mental well-being, Dr. Andreazza's work revolves around comprehending how mitochondrial function intersects with neurotransmission. With an overarching focus on mood disorders, her efforts are dedicated to enhancing the lives of individuals grappling with these challenges.Join us in this enlightening episode as we delve into the world of mitochondrial research and its potential to transform our understanding of mental health, guided by the remarkable insights and expertise of Dr. Ana Andreazza.On this Episode: Introduction to Dr. Ana Andreazza2:40 Dr. Ana Andreazza's Exploration Through Mitochondria, Energy, and Mental Health8:18 Journey from studying Oxidative Stress to Redefining Mental Well-being18:17 Mitochondrial Health and Overall Well-Being26:28 Diverse origins of Psychiatric disorders 30:36 Dr. Ana's Vision for Mitochondrial Medicine and Mito2i38:57 The Vital Connection Between Ketones and Brain Health Show Links:Link to Dr. Ana Andreazza's website links: https://mito2i.ca My website is: Call to action for listeners: Follow ketones and Coffee Podcast on Instagram ( https://www.instagram.com/keton.esncoffee ), Youtube ( https://www.youtube.com/channel/UCsZZmBEenvZnU8tA1npAODA ), and Twitter ( https://twitter.com/KetonesP ) for updates and new episodes.~~~~~~Estrella by Audiorezout is licensed under a Attribution-NonCommercial-ShareAlike 4.0 International License.~~~~~~ Save yourself that trip to the market — Instacart delivers groceries in as fast as 1 hour! They connect you with Personal Shoppers in your area to shop and deliver groceries from your favorite stores.Instacart - Groceries delivered in as little as 1 hour. Free delivery on your first order over $35. Go to ketocoachlorenz.com and use the contact form to get your Free Consultation!Support the show

I am thrilled to have Dr. Ana Andreazza, a distinguished professor at the University of Toronto, where she holds esteemed positions within the departments of Pharmacology and Toxicology, as well as Psychiatry. As the holder of a prestigious Canada Research Chair in Molecular Pharmacology of Mood Disorders, Dr. Andreazza's expertise delves into the intricate interplay between molecular pharmacology and mental health.At the forefront of groundbreaking research, Dr. Andreazza wears another significant hat as the Scientific Director of the Mitochondrial Innovation Initiative (Mito2i). Her remarkable contributions extend to the publication of over 150 research articles, garnering an impressive 9,000 citations. Dr. Andreazza's exceptional influence in the realm of mitochondrial research is particularly notable in its application to mental health, specifically mood disorders.Through her unwavering commitment to unraveling the mysteries of mitochondria and their profound impact on mental well-being, Dr. Andreazza's work revolves around comprehending how mitochondrial function intersects with neurotransmission. With an overarching focus on mood disorders, her efforts are dedicated to enhancing the lives of individuals grappling with these challenges.Join us in this enlightening episode as we delve into the world of mitochondrial research and its potential to transform our understanding of mental health, guided by the remarkable insights and expertise of Dr. Ana Andreazza.On this Episode: Introduction to Dr. Ana Andreazza2:40 Dr. Ana Andreazza's Exploration Through Mitochondria, Energy, and Mental Health8:18 Journey from studying Oxidative Stress to Redefining Mental Well-being18:17 Mitochondrial Health and Overall Well-Being26:28 Diverse origins of Psychiatric disorders 30:36 Dr. Ana's Vision for Mitochondrial Medicine and Mito2i38:57 The Vital Connection Between Ketones and Brain Health Show Links:Link to Dr. Ana Andreazza's website links: https://mito2i.ca My website is: Call to action for listeners: Follow ketones and Coffee Podcast on Instagram ( https://www.instagram.com/keton.esncoffee ), Youtube ( https://www.youtube.com/channel/UCsZZmBEenvZnU8tA1npAODA ), and Twitter ( https://twitter.com/KetonesP ) for updates and new episodes.~~~~~~Estrella by Audiorezout is licensed under a Attribution-NonCommercial-ShareAlike 4.0 International License.~~~~~~ Save yourself that trip to the market — Instacart delivers groceries in as fast as 1 hour! They connect you with Personal Shoppers in your area to shop and deliver groceries from your favorite stores.Instacart - Groceries delivered in as little as 1 hour. Free delivery on your first order over $35. Go to ketocoachlorenz.com and use the contact form to get your Free Consultation!Support the show

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.06.21.545967v1?rss=1 Authors: Boyd, S. L., Kuhn, N. C., Patterson, J. R., Stoll, A. C., Zimmerman, S. A., Kolanowski, M. R., Neubecker, J. J., Luk, K. C., Ramsson, E. S., Sortwell, C. E., Bernstein, A. I. Abstract: Parkinson's disease (PD) is the most common movement disorder and one of the fastest-growing neurological diseases worldwide. This increase outpaces the rate of aging and is most rapid in recently industrialized areas, suggesting the role of environmental factors. Consistent with this, epidemiological studies show an association between exposure to persistent organic pollutants and an increased risk of PD. When combined with post-mortem analysis and mechanistic studies, a role for specific compounds, including the organochlorine pesticide dieldrin, emerges. In mouse models, developmental dieldrin exposure causes male-specific exacerbation of neuronal susceptibility to MPTP and synucleinopathy. Specifically, our novel two-hit model combining developmental dieldrin exposure with the -synuclein (-syn) pre-formed fibril (PFF) model showed a male-specific exacerbation of PFF-induced increases in striatal dopamine (DA) turnover and motor deficits on the challenging beam 6 months post-PFF injection in male offspring developmentally exposed to dieldrin. Here, we hypothesized that alterations in DA handling contribute to the observed changes and assessed vesicular monoamine transporter 2 (VMAT2) function and DA release in this dieldrin/PFF two-hit model. Female C57BL/6 mice were exposed to 0.3 mg/kg dieldrin or vehicle every 3 days, starting at 8 weeks of age by feeding and continuing throughout breeding, gestation, and lactation. Male offspring from independent litters underwent unilateral, intrastriatal injections of -syn PFFs via stereotaxic surgery at 12 weeks of age and DA handling was assessed 4 months post-PFF injection via vesicular 3H-DA uptake assay and fast-scan cyclic voltammetry (FSCV). We observed no dieldrin-associated change in VMAT2 activity, but a dieldrin-induced increase in DA release in striatal slices in PFF-injected animals. These results suggest that developmental dieldrin exposure alters the dopaminergic response to synucleinopathy-triggered toxicity and supports our hypothesis that alterations in DA handling may underly the observed exacerbation of PFF-induced deficits in motor behavior and DA turnover. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

This episode covers some papers from January 2023 on treatments focused on repairing the neurotransmitter imbalance in Alzheimer's disease. We hope you enjoy listening as Christy summarizes this exciting research—from the discovery of new therapeutics to the synthesis of drugs. Sections in this episode:Drug Screening (3:37)New Drugs (7:00)Synthesized Drugs (13:35)-------------------------------------------------------------- To find the numbered bibliography with all the papers covered in this episode, click here, or use the link below:https://drive.google.com/file/d/1BkF6ofShRYL_ggRRFKvNsHvBz4PrLfXr/view?usp=share_linkTo access the folder with ALL our bibliographies, follow this link (it will be updated as we publish episodes and process bibliographies), or use the link below:https://drive.google.com/drive/folders/1bzSzkY9ZHzzY8Xhzt0HZfZhRG1Gq_Si-?usp=sharingYou can also find all of our bibliographies on our website: amindr.com. -------------------------------------------------------------- We at AMiNDR are eager to hear from you! We opened up a survey available until the end of April for you to tell us what we are doing well, and where we can improve. Access the survey at tinyurl.com/amindrsurvey. All survey responses will be anonymous. By doing the survey, you can choose to enter a draw for a $15USD gift card for any location you choose! -------------------------------------------------------------- Follow-up on social media for more updates!Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastFacebook:  AMiNDR  Youtube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us spread the word about AMiNDR to your friends, colleagues, and networks! And if you could leave us a rating and/or review on your streaming app of choice (Apple Podcasts, Spotify, or wherever you listen to the podcast), that would be greatly appreciated! It helps us a lot and we thank you in advance for leaving a review! Don't forget to subscribe to hear about new episodes as they come out too. Thank you to our sponsor, the Canadian Consortium of Neurodegeneration in Aging, or CCNA, for their financial support of this podcast. This helps us to stay on the air and bring you high quality episodes. You can find out more about the CCNA on their website: https://ccna-ccnv.ca/. Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted and hosted by Ellen Koch, edited by Michelle Grover, and reviewed by Christy Yu and Anusha Kamesh. The bibliography and wordcloud were created by Lara Onbasi (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For January 2023, the sorters were Elyn Rowe, Christy Yu, Eden Dubchak, Ben Cornish, Kevin Nishimura, Anelya Gandy, Salodin Al-Achkar, and Rob Cloke. Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, Lara Onbasi, Joseph Liang, and Judy Cheng, for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

Waffle Irongirl interviews Alex Mortensen on his writing on his lived experience of epilepsy. Alex has produced the Neurotransmission anthology featuring poetry, writing and art exploring this topic.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.16.528856v1?rss=1 Authors: Beitchman, J. A., Krishna, G., Bromberg, C. A., Thomas, T. C. Abstract: Aspects of glutamate neurotransmission implicated in normal and pathological conditions are often evaluated using in vivo recording paradigms in rats anesthetized with isoflurane or urethane. Urethane and isoflurane anesthesia influence glutamate neurotransmission through different mechanisms; however real-time outcome measures of potassium chloride (KCl)-evoked glutamate overflow and glutamate clearance kinetics have not been compared within and between regions of the brain. In the following experiments, in vivo amperometric recordings of KCl-evoked glutamate overflow and glutamate clearance kinetics (uptake rate and T80) in the cortex, hippocampus and thalamus were performed using glutamate-selective microelectrode arrays (MEAs) in young adult male, Sprague-Dawley rats anesthetized with isoflurane or urethane. Potassium chloride (KCl)-evoked glutamate overflow was similar under urethane and isoflurane anesthesia in all brain regions studied. Analysis of glutamate clearance determined that the uptake rate was significantly faster (53.2%, p less than 0.05) within the thalamus under urethane compared to isoflurane, but no differences were measured in the cortex or hippocampus. Under urethane, glutamate clearance parameters were region dependent, with significantly faster glutamate clearance in the thalamus compared to the cortex but not the hippocampus (p less than 0.05). No region dependent differences were measured for glutamate overflow using isoflurane. These data support that amperometric recordings of glutamate under isoflurane and urethane anesthesia result in mostly similar and comparable data. However, certain parameters of glutamate uptake vary based on choice of anesthesia and brain region. Special considerations must be given to these areas when considering comparison to previous literature and when planning future experiments. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.09.523312v1?rss=1 Authors: Green, M. V., Gallegos, D. A., Boua, J.-V., Bartelt, L. C., Narayanan, A., West, A. E. Abstract: Glutamatergic projection neurons of the lateral habenula (LHb) drive behavioral state modulation by regulating the activity of midbrain monoaminergic neurons. Identifying circuit mechanisms that modulate LHb output is of interest for understanding control of motivated behaviors. A small population of neurons within the medial subnucleus of the mouse LHb express the GABAergic synthesizing enzyme GAD2, and they can inhibit nearby LHb projection neurons; however, these neurons lack markers of classic inhibitory interneurons and they co-express the vesicular glutamate transporter VGLUT2. To determine the molecular phenotype of these neurons, we genetically tagged the nuclei of GAD2-positive cells and used fluorescence-activated nuclear sorting to isolate and enrich these nuclei for single nuclear RNA sequencing (FANS-snRNAseq). Our data confirm that GAD2+/VGLUT2+ neurons intrinsic to the LHb co-express markers of both glutamatergic and GABAergic transmission and that they are transcriptionally distinct from either GABAergic interneurons or habenular glutamatergic neurons. We identify gene expression programs within these cells that show sex-specific differences in expression and that are implicated in major depressive disorder (MDD), which has been linked to LHb hyperactivity. Finally, we identify the Ntng2 gene encoding the cell adhesion protein Netrin-G2 as a marker of LHb GAD2+/VGLUT+ neurons and a gene product that may contribute to their target projections. These data show the value of using genetic enrichment of rare cell types for transcriptome studies, and they advance understanding of the molecular composition of a functionally important class of GAD2+ neurons in the LHb. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.20.521193v1?rss=1 Authors: Seidenthal, M., Janosi, B., Rosenkranz, N., Schuh, N., Elvers, N., Willoughby, M., Zhao, X., Gottschalk, A. Abstract: pH-sensitive fluorescent proteins are widely used to study synaptic vesicle (SV) fusion and recycling. When targeted to the lumen of SVs, fluorescence of these proteins is quenched by the acidic pH. Following SV fusion, they are exposed to extracellular neutral pH, resulting in a fluorescence increase. SV fusion, recycling and acidification can thus be tracked by tagging integral SV proteins with pHsensitive proteins. Neurotransmission is generally stimulated by electrophysiology, which is not feasible in small, intact animals, thus limiting the approach to cell culture regimes. Previous in vivo approaches depended on distinct (sensory) stimuli, thus limiting the addressable neuron types. To overcome these limitations, we established an all-optical approach to stimulate and visualize SV fusion and recycling. We combined distinct pH-sensitive fluorescent proteins (inserted into the SV protein synaptogyrin) and light-gated channelrhodopsins (ChRs) for optical stimulation, overcoming optical crosstalk and thus enabling an all-optical approach. We generated two different variants of the pHsensitive optogenetic reporter of vesicle recycling (pOpsicle) and tested them in cholinergic neurons of intact Caenorhabditis elegans nematodes. First, we combined the red fluorescent protein pHuji with the blue-light gated ChR2(H134R), and second, the green fluorescent pHluorin combined with the novel red-shifted ChR ChrimsonSA. In both cases, fluorescence increases were observed after optical stimulation. Increase and subsequent decline of fluorescence was affected by mutations of proteins involved in SV fusion and endocytosis. These results establish pOpsicle as a non-invasive, all-optical approach to investigate different steps of the SV cycle. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.14.520496v1?rss=1 Authors: Balivada, S., Tapia, G. P., Pawar, H. N., Khan, A. M., Kenney, M. J. Abstract: The rostral ventrolateral medulla (RVLM), a part of the medullary reticular formation, plays a major role in several physiological responses, including cardiovascular and sympathetic nervous system functions. Although aging causes disturbances in the responses of these physiological systems, RVLM involvement in these age-related changes is not clear. Previous work using high-throughput gene expression analysis of the RVLM in aged animals suggested that chemical neurotransmission-related genes might be downregulated with advancing age. Since RVLM function involves a balance of signals from inhibitory and excitatory inputs, which is largely mediated by gamma-aminobutyric acid (GABA) and excitatory amino acid (EAA) neurotransmission, we hypothesized that aging is associated with altered excitatory and/or inhibitory neurotransmission-related gene expression in the RVLM. To test this hypothesis, we micropunched an RVLM-containing area from young (3-5 months), middle-aged (12-14 months), and aged (22-26 months) Fischer 344 male rats. RNA purified from these micropunches was analyzed using GABA and Glutamate RT2 Profiler PCR arrays (n= 8-10). Each profiler array has primers for 84 GABA and glutamate neurotransmission related genes. In addition, the expression of selected genes was validated at the RNA level using TaqMan(R) based- qPCR and at the protein level using western blotting. All the genes that displayed significant differential expression (1.5-fold, p less than .05, FDR less than .05) were identified to be downregulated in the RVLM of aged and middle-aged rats compared to young rats. This downregulation did not appear to be a result of RVLM tissue sampling differences among the age groups, since a separate validation of our sampling method, which involved careful mapping of micropunched regions to a standardized brain atlas, revealed no spatial differences in sampled sites among age groups. Among the downregulated genes, the percentage of glutamate neurotransmission-related genes was higher than GABA neurotransmission-related genes. The Solute carrier family 1 member 6 (Slc1a6) gene showed the highest fold downregulation at the RNA level in the RVLM of aged compared to young rats, and its protein product, Excitatory amino acid transporter 4 (EAAT4), showed a downregulatory trend in the RVLM of aged and middle-aged rats. These results suggest that molecular constituents of both GABA and glutamate neurotransmission might be altered in the RVLM of aged and middle-aged rats, and the changes in glutamate neurotransmission might be more prominent. Investigating age-associated anatomical and functional changes in RVLM GABA and glutamate neurotransmission might provide a foundation for understanding the effects of aging on physiological function. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.18.512779v1?rss=1 Authors: Shields, B. C., Yan, H., Lim, S. S. X., Burwell, S. C., Fleming, E. A., Cammarata, C. M., Kahuno, E. W., Vagadia, P. P., Loughran, M. H., Zhiquan, L., McDonnell, M. E., Scalabrino, M. L., Thapa, M., Hawley, T. M., Reitz, A. B., Schiltz, G. E., Hull, C., Field, G. D., Glickfeld, L. L., TADROSS, M. R. Abstract: Cell-specific pharmaceutical technologies promise mechanistic insight into clinical drugs[-]those that treat, and often define, human disease. In particular, DART (drug acutely restricted by tethering) achieves genetically programmable control of drug concentration over cellular dimensions. The method is compatible with clinical pharmaceuticals and amenable to studies in behaving animals. Here, we describe DART.2, comprising three advances. First, we improve the efficiency of chemical capture, enabling cell-specific accumulation of drug to ~3,000-times the ambient concentration in 15 min. Second, we develop tracer reagents, providing a behavior- independent measure of cellular target engagement in each animal. Third, we extend the method to positive allosteric modulators and outline design principles for this clinically significant class. We showcase the platform with four pharmaceuticals[-]two that weaken excitatory (AMPAR) or inhibitory (GABAAR) chemical neurotransmission, and two that strengthen these forms of synaptic communication. Across four labs, we tested reagents in the mouse cerebellum, basal ganglia, visual cortex, and retina. Collectively, we demonstrate robust, bidirectional editing of chemical neurotransmission. We provide for distribution of validated reagents, community design principles, and synthetic building blocks for application to diverse pharmaceuticals. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.03.510559v1?rss=1 Authors: Okada, S., Kobayashi, M., Lee, H., Morita, M. Abstract: The brain abundantly expresses adenosine receptors, which are involved in the regulation of neural activity, blood flow, and inflammation. In a previous study using our originally developed adenosine biosensor, we reported that hippocampal astrocytes release ATP upon water influx from the water channel AQP4, which is degraded extracellularly to increase adenosine (Yamashiro et al., 2017). On the other hand, the interaction between adenosine and dopamine is widely known, and when adenosine release from astrocytes is altered by inflammation or other factors, abnormal dopamine neurotransmission and related ataxia and psychiatric disorders may develop. In the present study, we examined pathological changes in adenosine or dopamine release in depressive-like behavior that develops as a symptom of cocaine withdrawal. The results showed that A1 receptor inhibitors and AQP4 gene disruption suppressed depressive-like behavior. In the striatum, AQP4-dependent adenosine release inhibited dopamine release via A1 receptors, and cocaine inhibited dopamine release by increasing this adenosine release. In contrast, in the medial frontal cortex, AQP4-dependently released adenosine enhanced dopamine release via A1 receptors, and cocaine abolished this adenosine effect. Furthermore, adenosine action was restored in AQP4 knockout mice, suggesting that cocaine reduced A1 receptor function via AQP4-dependent adenosine. In conclusion, astrocytes modulate dopaminergic neurotransmission through AQP4-mediated adenosine release, and this disruption leads to depression-like behavior. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.06.506833v1?rss=1 Authors: Kang, W. K., Araya, A., Fox, B. W., Thackeray, A., Schroeder, F. C., Walhout, A. J. M., Alkema, M. J. Abstract: A growing body of evidence indicates that gut microbiota influence brain function and behavior. However, the molecular basis of how gut bacteria modulate host nervous system function is largely unknown. Here we show that vitamin B12-producing bacteria that colonize the intestine can modulate excitatory synaptic transmission and behavior in the host Caenorhabditis elegans. We find that vitamin B12 reduces cholinergic signaling in the nervous system through rewiring of the methionine (Met)/S-Adenosylmethionine (SAM) cycle in the intestine. We identify a conserved metabolic crosstalk between the Met/SAM cycle and the choline oxidation pathway. We show that metabolic rewiring of these pathways by vitamin B12 reduces cholinergic transmission by limiting the availability of free choline required by neurons to synthesize acetylcholine. Our study reveals a gut-brain communication pathway by which enteric bacteria modulate host behavior and may affect mental health. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

We start off our January 2022 series of AMiNDR with this episode highlighting 9 papers on changes to synaptic transmission in Alzheimer's Disease. In this episode, Anusha will cover topics including changes to GABAergic and glutamatergic transmission and calcium flux in AD-affected neurons. We also have papers looking at age-dependent changes in synaptic function in AD. End neuro-transmission ;) Sections in this episode:  Changes to GABAergic transmission (2.41)  Changes to calcium flux (6.42)  Changes to glutamateric transmission (8.38)  Age-dependent changes in AD (13.11) -------------------------------------------------------------- To find the numbered bibliography with all the papers covered in this episode, click here, or use the link below:https://drive.google.com/file/d/1hUH8nXFf-O73pJlkHH4u9d0kBb3ibNUZ/view?usp=sharingTo access the folder with ALL our bibliographies, follow this link (it will be updated as we publish episodes and process bibliographies), or use the link below:https://drive.google.com/drive/folders/1bzSzkY9ZHzzY8Xhzt0HZfZhRG1Gq_Si-?usp=sharingYou can also find all of our bibliographies on our website: www.amindr.com. --------------------------------------------------------------Follow-up on social media for more updates!Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastFacebook:  AMiNDR  Youtube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us spread the word about AMiNDR to your friends, colleagues, and networks! And if you could leave us a rating and/or review on your streaming app of choice (Apple Podcasts, Spotify, or wherever you listen to the podcast), that would be greatly appreciated! It helps us a lot and we thank you in advance for leaving a review! Don't forget to subscribe to hear about new episodes as they come out too. Thank you to our sponsor, the Canadian Consortium of Neurodegeneration in Aging, or CCNA, for their financial support of this podcast. This helps us to stay on the air and bring you high quality episodes. You can find out more about the CCNA on their website: https://ccna-ccnv.ca/. Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted, hosted and edited by Anusha Kamesh, and reviewed by Christy Yu and Ellen Koch. The bibliography was made by Anjana Rajendran and the wordcloud was created by Sarah Louadi (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For January 2022, the sorters were Jacques Ferreira, Christy Yu, Kate Van Pelt, Kira Tosefsky, Dana Clausen, Eden Dubchak, Ben Cornish, Elyn Rowe and Ellen Koch. Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, and Jacques Ferreira for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

17 papers have "Targeting neurotransmission and synaptic dysfunction in AD" written all over it. Figuratively speaking of course. Anusha covers topics like targeting neurotoxicity and calcium flux, or acetylcholine transmission and balance, or even targeting monoamine oxidases to improve AD-like pathology. Better yet, this episode lets you keep up to date as all the papers were published in November of 2021.  Sections in this episode:  Targeting synaptic dysfunction (2.34)  Targeting M1 acetylcholine receptors (14.03)  Targeting cholinesterases by modifying existing drugs (17.32)  Targeting cholinesterases with novel drugs (22.49)  Targeting monoamine oxidases (27.31) -------------------------------------------------------------- To find the numbered bibliography with all the papers covered in this episode, click here, or use the link below:https://drive.google.com/file/d/1cNr1Wd34FaDep1FfTuVaBqzLzcQapYeh/view?usp=sharingTo access the folder with all the bibliographies for 2021 papers, follow this link (it will be updated as we publish episodes and process bibliographies), or click the following link below:https://drive.google.com/drive/folders/1N1zx_itPkCDNYE1yFGZzQxDDR-NiRx3p?usp=sharingYou can also find all of our bibliographies on our website: www.amindr.com. --------------------------------------------------------------Follow-up on social media for more updates!Facebook:  AMiNDR  Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastYoutube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us by spreading the word about AMiNDR to your friends, colleagues, and networks! Another way you can help us reach more listeners who would benefit from the show is by rating and/or reviewing us on Apple Podcasts, Spotify,  or wherever you listen to podcasts. It helps us a lot and we thank you in advance for leaving a review! Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted, hosted and edited by Anusha Kamesh, and reviewed by Ellen Koch. The bibliography was made by Lara Onbasi, and the wordcloud was created by Sarah Louadi (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For November 2021, the sorters were Jacques Ferreira, Christy Yu, Kate Van Pelt, Kira Tosefsky, Dana Clausen, Nicole Corso, Eden Dubchak, Ben Cornish, Ellen Koch, Elyn Rowe, and Naila KuhlmannAlso, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, Jacques Ferreira for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

Neuroplasticity, or the ability of the brain to change, is a huge term that encompasses all the things that make humans who they are. It is why some deaf people are more sensitive to vibrations and body language. The stroke patient who suffers aphasia sometimes learns to speak again. It is how people learn after … Continue reading Neurotransmission, Neuroplasticity, and an Origin Story

Thinking about thinking? Changes to synaptic transmission contribute to Alzheimer's disease pathology. Hear all about 10 papers published in October of 2021 exploring synaptic dysfunction in AD from Anusha who hosts this episode.  Sections in this episode:  Synaptic dysfunction in rodent AD models (2.58)  Synaptic dysfunction in other AD models & human studies (16.41) -------------------------------------------------------------- You can find the numbered bibliography for this episode by clicking here, or the link below: https://drive.google.com/file/d/1LYhcoVeGPq5QEWzCqqDCvJsOgMdo3jKt/view?usp=sharingTo access the folder with all the bibliographies for 2021 papers so far, follow this link (it will be updated as we publish episodes and process bibliographies), or click the following link below:https://drive.google.com/drive/folders/1N1zx_itPkCDNYE1yFGZzQxDDR-NiRx3p?usp=sharingYou can also join our mailing list to receive a newsletter by filling this form. --------------------------------------------------------------Follow-up on social media for more updates!Facebook:  AMiNDR  Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastYoutube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us by spreading the word about AMiNDR to your friends, colleagues, and networks! Another way you can help us reach more listeners who would benefit from the show is by leaving us a review on Apple Podcasts or wherever you listen to podcasts. It helps us a lot and we thank you in advance for leaving a review! Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted, hosted and edited by Anusha Kamesh, and reviewed by Ellen Koch. The bibliography was generated by Lara Onbasi and the wordcloud was created by Sarah Louadi (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For October 2021, the sorters were Jacques Ferreira, Christy Yu, Kate Van Pelt, Eden Dubchak, Kira Tosefsky, Dana Clausen, Ellen Koch and Elyn Rowe.Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, Jacques Ferreira, and Shruti Kocchar for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   Our sponsor, the Canadian Consortium of Neurodegeneration in Aging, has provided financial support to our podcast that helps us to purchase software, recording equipment, distribution services, and more. To find out more about the CCNA, you can visit their website at https://ccna-ccnv.ca/. -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

Hello there! Just in time for the holiday season we've got quite the deal lined up for you. Two episodes for the length of one! Anusha will be guiding you through the literature of October 2021 that focuses on targeting neuronal function and neurotransmission as an Alzheimer's disease treatment. If you want to find out the progress we've been making as a field towards finding better treatments, this is the episode for you!  Sections in this episode:  Targeting neuronal and synaptic protection (2.33)  Targeting neurotransmission (13.27) -------------------------------------------------------------- You can find the numbered bibliography for this episode by clicking here, or the link below: https://drive.google.com/file/d/1UK_5b07HLhanVYgDN8mbIsIBkmB24kOh/view?usp=sharingTo access the folder with all the bibliographies for 2021 so far, follow this link (it will be updated as we publish episodes and process bibliographies), or click the following link below:https://drive.google.com/drive/folders/1N1zx_itPkCDNYE1yFGZzQxDDR-NiRx3p?usp=sharingYou can also join our mailing list to receive a newsletter by filling this form. Or tweet at us: @AMiNDR_podcast  --------------------------------------------------------------Follow-up on social media for more updates!Facebook:  AMiNDR  Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastYoutube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us by spreading the word about AMiNDR to your friends, colleagues, and networks! Another way you can help us reach more listeners who would benefit from the show is by leaving us a review on Apple Podcasts or wherever you listen to podcasts. It helps us a lot and we thank you in advance for leaving a review! Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted, hosted and edited by Anusha Kamesh, and reviewed by Christy Yu and Ellen Koch. The bibliography was generated by Lara Onbasi and the wordcloud was created by Sarah Louadi (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For October 2021, the sorters were Jacques Ferreira, Christy Yu, Kate Van Pelt, Eden Dubchak, Kira Tosefsky, Dana Clausen, Ellen Koch and Elyn Rowe.Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, Jacques Ferreira, and Shruti Kocchar for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

18 papers published in September of 2021 await you. What do they all have in common? They explore treatments for Alzheimer's disease that all target neurotransmission. If you're interested in restoring acetylcholine balance or other treatments that also improve cognitive function in Alzheimer's disease, tune in to hear Anusha take you through the literature.  Sections in this episode:  Discovery and synthesis of novel cholinesterase inhibitors (3.17)  Tacrine-based cholinesterase inhibitors (11.26)  Modifying existing treatments (16.16)  Multi-target treatments (23.00)  -------------------------------------------------------------- You can find the numbered bibliography for this episode by clicking here, or the link below:https://drive.google.com/file/d/1W--JfD89cCJWVbOrdFKCiZTI6cWrO54X/view?usp=sharingTo access the folder with all the bibliographies for 2021 so far, follow this link (it will be updated as we publish episodes and process bibliographies), or click the following link below:https://drive.google.com/drive/folders/1N1zx_itPkCDNYE1yFGZzQxDDR-NiRx3p?usp=sharingYou can also join our mailing list to receive a newsletter by filling this form. Or tweet at us: @AMiNDR_podcast  --------------------------------------------------------------Follow-up on social media for more updates!Facebook:  AMiNDR  Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastYoutube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us by spreading the word about AMiNDR to your friends, colleagues, and networks! Another way you can help us reach more listeners who would benefit from the show is by leaving us a review on Apple Podcasts or wherever you listen to podcasts. It helps us a lot and we thank you in advance for leaving a review! Our team of volunteers works tirelessly each month to bring you every episode of AMiNDR. This episode was scripted, hosted and edited by Anusha Kamesh, and reviewed by Naila Kuhlmann and Ellen Koch. The bibliography and wordcloud were created by Sarah Louadi (www.wordart.com). Big thanks to the sorting team for taking on the enormous task of sorting all of the Alzheimer's Disease papers into episodes each month. For September 2021, the sorters were Jacques Ferreira, Ellen Koch, Christy Yu, Sarah Louadi, Kate Van Pelt, Nicole Corso, Eden Dubchak, Kira Tosefsky, Dana Clausen, and Elyn Rowe.Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, Jacques Ferreira, and Shruti Kocchar for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

This is an episode that explores the creation and testing of drugs that aim to restore neurotransmitter balance in Alzheimer's disease. It covers 14 papers that were all published in August of 2021, and Anusha will guide you through papers on targets including cholinesterases, serotonin, and glutamate receptors. Hit that play button if you'd like to hear more.  Sections in this episode:  Targeting acetylcholine with novel compounds (2.29)  Other targets with novel compounds (13.23)  Testing for or improving upon existing ACE inhibitors (17.28)   -------------------------------------------------------------- You can find the numbered bibliography for this episode by clicking here, or the link below:https://drive.google.com/file/d/1IIilzUhWAF_WuBM4trkcW12daiB52sT2/view?usp=sharingTo access the folder with all the bibliographies for 2021 so far, follow this link (it will be updated as we publish episodes and process bibliographies), or click the following link below:https://drive.google.com/drive/folders/1N1zx_itPkCDNYE1yFGZzQxDDR-NiRx3p?usp=sharingYou can also join our mailing list to receive a newsletter by filling this form. Or tweet at us: @AMiNDR_podcast  --------------------------------------------------------------Follow-up on social media for more updates!Facebook:  AMiNDR  Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastYoutube: AMiNDR PodcastLinkedIn: AMiNDR PodcastEmail: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us by spreading the word about AMiNDR to your friends, colleagues, and networks! Another way you can help us reach more listeners who would benefit from the show is by leaving us a review on Apple Podcasts or wherever you listen to podcasts. It helps us a lot and we thank you in advance for leaving a review! Our team of volunteers works together to bring you every episode of AMiNDR. In particular, this episode was scripted, hosted and edited by Anusha Kamesh, and reviewed by Naila Kuhlmann and Ellen Koch. The bibliography was made by Lara Onbasi and the wordcloud was created by Sarah Louadi (www.wordart.com). Big thanks to the sorting team for sorting all the papers published in August 2021 into themes for our episodes: Jacques Ferreira, Ellen Koch, Nicole Corso, Kate Van Pelt, Christy Yu, and Dana Clausen. Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, and Jacques Ferreira, for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, audio editing, creating bibliographies, and outreach/marketing. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

Journey through the entire spectrum of drug development as Anusha guides you through 19 papers that were published in July of 2021. We span research that begins with drug discovery all the way to the end goal: Phase II clinical trials. If you're interested in targeting levels of acetylcholine and monoamines, you're really going to like this episode!  Sections in this episode:  Synthesis and Discovery of Cholinesterase Inhibitors (2.47)  Drug Interactions with Multiple targets (9.29)  Pre-clinical Trials (18.23)  Clinical Trials (25.39)  -------------------------------------------------------------- You can find the numbered bibliography for this episode by clicking here, or the link below:https://drive.google.com/file/d/1uxRxoLdg_lmcLTrTJv9WsovybVL-0kMr/view?usp=sharingTo access the folder with all the bibliographies for 2021 so far, follow this link (it will be updated as we publish episodes and process bibliographies), or click the following link below:https://drive.google.com/drive/folders/1N1zx_itPkCDNYE1yFGZzQxDDR-NiRx3p?usp=sharingYou can also join our mailing list to receive a newsletter by filling this form. Or tweet at us: @AMiNDR_podcast  --------------------------------------------------------------Follow-up on social media for more updates!Facebook:  AMiNDR  Twitter: @AMiNDR_podcastInstagram: @AMiNDR.podcastYoutube: AMiNDR PodcastLinkedIn: AMiNDR PodcastIf you have any questions or concerns, do not hesitate to contact us at: amindrpodcast@gmail.com  -------------------------------------------------------------- Please help us by spreading the word about AMiNDR to your friends, colleagues, and networks! Another way you can help us reach more researchers is by leaving us a review on Apple Podcasts or wherever you listen to podcasts. It helps us a lot and we thank you in advance for leaving a review! Every episode of AMiNDR is the result of a huge team effort. Today's episode was scripted, hosted and edited by Anusha Kamesh, and reviewed by Glory Nasseri and Ellen Koch. The wordcloud (wordart.com) was generated by Sarah Louadi and the bibliography was created by Jacques Ferreira. Big thanks to the sorting team for sorting all the papers published in July into themes for our episodes: Jacques Ferreira, Elyn Rowe, Ellen Koch, Christy Yu, Nicole Corso, Sarah Louadi, and Naila Kuhlmann. Also, props to our management team, which includes Sarah Louadi, Ellen Koch, Naila Kuhlmann, Elyn Rowe, Anusha Kamesh, and Jacques Ferreira, for keeping everything running smoothly.Our music is from "Journey of a Neurotransmitter" by musician and fellow neuroscientist Anusha Kamesh; you can find the original piece and her other music on soundcloud under Anusha Kamesh or on her YouTube channel, AKMusic.   https://www.youtube.com/channel/UCMH7chrAdtCUZuGia16FR4w   -------------------------------------------------------------- If you are interested in joining the team, send us your CV by email. We are specifically looking for help with sorting abstracts by topic, abstract summaries and hosting, creating bibliographies, and promotions. However, if you are interested in helping in other ways, don't hesitate to apply anyways.  --------------------------------------------------------------*About AMiNDR: *  Learn more about this project and the team behind it by listening to our first episode: "Welcome to AMiNDR!" 

A  neurochemical thing. 

Welcome to Your Upgraded Summer!This new series revisits the Top 10 Bulletproof Radio episodes of all time. The topics cover essentials like nutrition, energy, hormones, sleep and autophagy, as well as gut, brain, autoimmune and women's health.You'll get the main points in a shortened version so you can get the good stuff and get on with your summer plans. And if you want to listen to more, tune in to the original episode.William Walsh, Ph.D., takes the No. 10 spot: Tailor Your Brain's Neurotransmission with Nutrients — William J. Walsh, Ph.D. #567In this revamped episode of Bulletproof Radio, I talk with research scientist Dr. Bill Walsh about how brain cells function, how they're nourished, and what we need to clear out our brain's trash and keep the good stuff around. He's spent over three decades studying how you can use nutrients and foods to improve your brain health. His expertise shows how mental health can be improved with nutritional psychiatry.More than 100 neurotransmitters in the brain act as chemical messengers. Research shows us that with certain nutrients you can directly affect how those neurotransmitters work. For people who struggle with addiction, for people who have a mental illness, for those who want to live longer, improve their memory and so much more, Dr. Walsh walks you through the nutrients that can make a difference.New research over the past decade shows us what protects our mind and body, and how much our environment influences that. Here's more of what Bill discovered:“Neuroscience advances and my interest has always been on the brain and on people with brain disorders, depression, anxiety, autism, schizophrenia--the whole litany of brain science. And my focus has to be on the neurotransmitters themselves. There are about five or six that seem to be especially important in mental disorders. For the first time in the last 10 years, we now are able with nutrients to directly affect neurotransmission of many of the most important neurotransmitters.” “It seems like all the research is still aimed at finding the next billion-dollar drug that can help people. And we now have enough knowledge that from the new research, when you put it all together, we're learning that with nutrients and with diet even, we can make radical improvements in people with depression and anxiety and problems like that. And that we don't necessarily need a drug.” “If you're going to do one test, do a zinc test. Because if you're low in zinc, that means your chance of getting cancer, chance of developing dementia, chance of developing heart disease is much greater. I would guess that probably half of Americans would benefit from more zinc.”Enjoy! And get more resources at Dave.Asprey/podcasts.Got a comment, idea or question for the podcast? Submit via this form.CHECK OUT OUR EPISODE PARTNER!The wearable Hapbee aligns your mental state with your goals. Go to https://hapbee.com/DAVE7TH ANNUAL BIOHACKING CONFERENCE: SEPTEMBER 17-19, 2021: https://www.biohackingconference.comDAVE ASPREY BOX: https://daveaspreybox.com/UPGRADE YOURSELF WITH DAVE ASPREY: https://ourupgradecollective.comSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Welcome to Your Upgraded Summer!This new series revisits the Top 10 Bulletproof Radio episodes of all time. The topics cover essentials like nutrition, energy, hormones, sleep and autophagy, as well as gut, brain, autoimmune and women's health.You'll get the main points in a shortened version so you can get the good stuff and get on with your summer plans. And if you want to listen to more, tune in to the original episode.William Walsh, Ph.D., takes the No. 10 spot: Tailor Your Brain's Neurotransmission with Nutrients — William J. Walsh, Ph.D. #567In this revamped episode of Bulletproof Radio, I talk with research scientist Dr. Bill Walsh about how brain cells function, how they're nourished, and what we need to clear out our brain's trash and keep the good stuff around. He's spent over three decades studying how you can use nutrients and foods to improve your brain health. His expertise shows how mental health can be improved with nutritional psychiatry.More than 100 neurotransmitters in the brain act as chemical messengers. Research shows us that with certain nutrients you can directly affect how those neurotransmitters work. For people who struggle with addiction, for people who have a mental illness, for those who want to live longer, improve their memory and so much more, Dr. Walsh walks you through the nutrients that can make a difference.New research over the past decade shows us what protects our mind and body, and how much our environment influences that. Here's more of what Bill discovered:“Neuroscience advances and my interest has always been on the brain and on people with brain disorders, depression, anxiety, autism, schizophrenia--the whole litany of brain science. And my focus has to be on the neurotransmitters themselves. There are about five or six that seem to be especially important in mental disorders. For the first time in the last 10 years, we now are able with nutrients to directly affect neurotransmission of many of the most important neurotransmitters.” “It seems like all the research is still aimed at finding the next billion-dollar drug that can help people. And we now have enough knowledge that from the new research, when you put it all together, we're learning that with nutrients and with diet even, we can make radical improvements in people with depression and anxiety and problems like that. And that we don't necessarily need a drug.” “If you're going to do one test, do a zinc test. Because if you're low in zinc, that means your chance of getting cancer, chance of developing dementia, chance of developing heart disease is much greater. I would guess that probably half of Americans would benefit from more zinc.”Enjoy! And get more resources at Dave.Asprey/podcasts.Got a comment, idea or question for the podcast? Submit via this form.CHECK OUT OUR EPISODE PARTNER!The wearable Hapbee aligns your mental state with your goals. Go to https://hapbee.com/DAVE7TH ANNUAL BIOHACKING CONFERENCE: SEPTEMBER 17-19, 2021: https://www.biohackingconference.comDAVE ASPREY BOX: https://daveaspreybox.com/UPGRADE YOURSELF WITH DAVE ASPREY: https://ourupgradecollective.comSee Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

Abelard Lindsay is a software developer and brain hacker, who's well-known in the biohacking community for formulating the CILTEP nootropic product, along with a line of Brain Food supplements, which contain the precursors needed to create various different neurotransmitters. Abelard is currently the Director of Research And Development at Natural Stacks.http://www.abelardresearch.comhttps://www.naturalstacks.com

Journal of Neurochemistry, Volume: 146, Issue: 4, Pages: 416-428, First published: 20 May 2018, DOI: (10.1111/jnc.14464) Life Sci . 2019 Sep 1;232:116612 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support

Through this audio series, we will try to understand the mechanisms by which our body communicates to the brain about the changes in external and internal environment by responding to the specific touch, pain and temperature stimuli. I believe this podcast is useful to you. All suggestions are welcome.

Join us as we discuss neurochemical triggers for vomiting, Ben Shapiro, reality TV and more. Music: A Really Good Time by Warren Malone warrenmalone.bandcamp.com Telephone Call by Jo Kroger jokroger.bandcamp.com Venus Orbit by The Synesthetic synesthetic.bandcamp.com Get the uncut version and loads more post-apocalyptic/speculative content at https://patreon.com/ewharrismusic --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app --- Send in a voice message: https://anchor.fm/wastelandentertainment/message

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.21.348995v1?rss=1 Authors: Liput, D. J., Puhl, H. L., Dong, A., He, K., Li, Y., Lovinger, D. M. Abstract: Several forms of endocannabinoid (eCB) signaling have been described in the dorsal lateral striatum (DLS), however most experimental protocols used to induce plasticity do not recapitulate the firing patterns of striatal-projecting pyramidal neurons in the cortex or firing patterns of striatal medium spiny neurons. Therefore, it is unclear if current models of eCB signaling in the DLS provide a reliable description of mechanisms engaged under physiological conditions. To address this uncertainty, we investigated mechanisms of eCB mobilization following brief synaptic stimulation that mimics in vivo patterns of neural activity in the DLS. To monitor eCB mobilization, the novel genetically encoded fluorescent eCB biosensor, GRABeCB2.0, was expressed in corticostriatal afferents of C57BL6J mice and evoked eCB transients were measured in the DLS using a brain slice photometry technique. We found that brief bouts of synaptic stimulation induce long lasting eCB transients. Inhibition of monoacylglycerol lipase, prolonged the duration of the eCB transient, while inhibition of diacylglycerol lipase inhibited the peak amplitude, suggesting that 2-AG is the predominate eCB generated following brief synaptic stimulation. 2-AG transients were robustly inhibited by AMPA and NMDA receptor antagonists, DNQX and DL-AP5 respectively. Additionally, the 2-AG transient was inhibited by the muscarinic M1 receptor (M1R) antagonist, VU 0255035, and augmented by the M1R positive allosteric modulator, VU 0486846, indicating that acetylcholine (ACh) release is required for efficient 2-AG production. The dopamine D2 receptor (D2R) agonist, quinpirole, inhibited the 2-AG transient. However, in slices from mice lacking D2Rs on cholinergic interneurons (CINs), quinpirole did not inhibit the 2-AG transient, demonstrating that D2Rs on CINs can modulate 2-AG production. The AMPA receptor or NMDA receptor antagonists, DNQX or DL-AP5 respectively, occluded 2-AG augmentation by VU 0486846 suggesting that converging glutamatergic and cholinergic signals are required for efficient 2-AG production following brief synaptic stimulation. Collectively, these data uncover unrecognized mechanisms underlying 2-AG mobilization in the DLS. Copy rights belong to original authors. Visit the link for more info

This episode covers content during Week 5 -- Monday, 10/5 through Friday, 10/9. The content specifically outlines the Nervous System -- with biology background, neuroanatomy, neurotransmission, neurotransmitters, organization of the Nervous System and lastly gets into the Endocrine System with hormones. This week is pretty intense, bio-wise. We will incorporate lots of practice in class and I will give you resources to guide you. You will also be given helpful charts/info to help chunk and organize this information. We got this!

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.18.302943v1?rss=1 Authors: Garcia Guerra, S., Spadoni, A., Mitchell, J., Strigo, I. A. Abstract: Molecular mechanisms of the interaction between pain and reward associated with pain relief processes in the human brain are still incompletely understood. This is partially due to the invasive nature of the available techniques to visualize and measure metabolic activity. Positron Emission Tomography (PET) radioligand studies using radioactive substances are still the only available modality to date that allows for the investigation of the molecular mechanisms in the human brain. For pain and reward studies, the most commonly studied PET radiotracers are [11C]-carfentanil (CFN) and [11C]- or [18F]-diprenorphine (DPN), which bind to opioid receptors, and [11C]-raclopride (RAC) and [18F]-fallypride (FAL) tracers, which bind to dopamine receptors. The current meta-analysis looks at 15 pain-related studies using opioid radioligands and 8 studies using dopamine radioligands in an effort to consolidate the available data into the most likely activated regions. Our primary goal was to identify regions of shared opioid/dopamine neurotransmission during pain-related experiences. SDM analysis of previously published voxel coordinate data showed that opioidergic activations were strongest in the bilateral caudate, thalamus, right putamen, cingulate gyrus, midbrain, inferior frontal gyrus, and left superior temporal gyrus. The dopaminergic studies showed that the bilateral caudate, thalamus, right putamen, cingulate gyrus, and left putamen had the highest activations. We were able to see a clear overlap between opioid and dopamine activations in a majority of the regions during pain-related processing, though there were some unique areas of dopaminergic activation such as the left putamen. Regions unique to opioidergic activation include the midbrain, inferior frontal gyrus, and left superior temporal gyrus. By investigating the regions of dopaminergic and opioidergic activation, we can potentially provide more targeted treatment to these sets of receptors in patients with pain conditions. These findings could eventually assist in the development of more targeted medication in order to help treat pain conditions and simultaneously prevent physical dependency. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.10.291963v1?rss=1 Authors: Thomas, C. S., Rana, M., Qiao, M., Borgland, S. L. Abstract: Reward and reinforcement processes are critical for survival and propagation of genes. While numerous brain systems underlie these processes, a cardinal role is ascribed to mesolimbic dopamine. However, ventral tegmental area (VTA) dopamine neurons receive complex innervation and various neuromodulatory factors, including input from lateral hypothalamic orexin/hypocretin neurons which also express and co-release the neuropeptide, dynorphin (LHox/dyn). Dynorphin in the VTA induces aversive conditioning through the Kappa opioid receptor (KOR) and decreases dopamine when administered intra-VTA. Exogenous application of orexin or orexin 1 receptor (OXR1) antagonists in the VTA bidirectionally modulates dopamine-driven motivation and reward-seeking behaviours, including the attribution of motivational value to primary rewards and associated conditioned stimuli. However, the effect of endogenous stimulation of LHox/dyn-containing projections to the VTA and the potential contribution of co-released dynorphin on mesolimbic dopamine and reward related processes remains uncharacterised. We combined optogenetic, electrochemical, and behavioural approaches to examine this. We found that optical stimulation of LHox/dyn inputs in the VTA potentiates mesolimbic dopamine neurotransmission in the nucleus accumbens (NAc) core, produces real time and place preference, and increases the incentive value attributed to a Pavlovian food cue. LHox/dyn potentiation of NAc dopamine release and real time place preference was completely blocked by an OXR1 antagonist. Thus, rewarding effects associated with optical stimulation of LHox/dyn inputs in the VTA are predominantly driven by orexin rather than dynorphin. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.29.273482v1?rss=1 Authors: Gomez, J. L., Bonaventura, J., Keighron, J., Wright, K. M., Marable, D. L., Rodriguez, L. A., Lam, S., Carlton, M. L., Ellis, R. J., Jordan, C., Bi, G.-H., Pignatelli, M., Bannon, M. J., Xi, Z.-X., Tanda, G., Michaelides, M. Abstract: Cocaine binds to the dopamine transporter (DAT) in the striatum to regulate cocaine reward and seeking behavior. Zinc (Zn2+) also binds to the DAT, but the in vivo relevance of this interaction is unknown. We found that cocaine abuse in humans correlated with low postmortem striatal Zn2+ content. In mice, cocaine decreased striatal vesicular Zn2+ and increased striatal synaptic Zn2+ concentrations and Zn2+ uptake. Striatal synaptic Zn2+ increased cocaine's in vivo potency at the DAT and was required for cocaine-induced DAT upregulation. Finally, genetic or dietary Zn2+ manipulations modulated cocaine locomotor sensitization, conditioned place preference, self-administration, and reinstatement. These findings reveal new insights into cocaine's pharmacological mechanism of action and indicate that Zn2+ can serve as a critical environmentally derived regulator of human cocaine addiction. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.28.271742v1?rss=1 Authors: Grasskamp, A. T., Jusyte, M., McCarthy, A. W., Goetz, T. W. B., Walter, A. M. Abstract: Synaptic transmission relies on presynaptic neurotransmitter (NT) release from synaptic vesicles (SVs), and on NT detection by postsynaptic receptors. Two principal modes exist: action-potential (AP) evoked and AP-independent "spontaneous" transmission. Though universal to all synapses and essential for neural development and function, regulation of spontaneous transmission remains enigmatic. Mechanisms divergent from AP-evoked transmission were described, but are difficult to reconcile with its established function in adjusting AP-evoked transmission. By studying neurotransmission at individual synapses of Drosophila larval neuromuscular junctions (NMJs), we show a clear interdependence of transmission modes: Components of the AP-evoked NT-release machinery (Unc13, Syntaxin-1 and BRP) also predicted spontaneous transmission. Both modes were reduced when blocking voltage-gated calcium channels and engaged an overlapping pool of SVs and NT-receptors. While a small subset (~21%) of spontaneously active synapses appeared limited to this mode, most also mediated AP-evoked transmission and activity was highly correlated. Thus, by engaging overlapping molecular machinery, spontaneous transmission predicts AP-evoked transmission at single synapses. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.19.255794v1?rss=1 Authors: Hmaied, C., Koulchitsky, S., Gladwyn-Ng, I., Seutin, V. Abstract: Although the fast antidepressant effect of ketamine is now well established clinically, neither its mechanism(s) nor its main site(s) of action is clearly defined. Because enhanced serotoninergic (5-HT) transmission is an important part of the antidepressant effect of various drug classes, we asked whether ketamine and one of its metabolites (hydroxynorketamine [HNK]), both used in their racemic form, may modulate the excitatory drive onto these neurons. Using whole-cell recordings from pharmacologically identified 5-HT and non-5-HT neurons in juvenile rat dorsal raphe slices, we found that both ketamine and HNK (10 microM) increase excitatory AMPA neurotransmission onto a subset (50%) of 5-HT neurons, whereas other 5-HT cells were unaffected. Both compounds increased the amplitude as well as the frequency of spontaneous excitatory post-synaptic currents (sEPSCs) mediated by AMPA receptors. The effect of ketamine was more robust than the one of HNK, since it significantly enhanced the charge transfer through AMPA channels, whereas HNK did not. The increase in the excitatory drive induced by ketamine was dependent on NMDA receptor blockade. In the presence of tetrodotoxin, the effect of ketamine was markedly reduced. Non-5-HT neurons, on the other hand, were unaffected by the drugs. We conclude that ketamine and HNK increase the excitatory drive onto a subset of 5-HT neurons by promoting glutamate release and possibly also through a postsynaptic action. The effect of ketamine is dependent on NMDA receptor modulation and appears to involve a network effect. These findings improve our understanding of the fast-acting antidepressant effect of ketamine. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.06.189522v1?rss=1 Authors: Kuijpers, M., Kochlamazashvili, G., Stumpf, A., Puchkov, D., Lucht, M. T., Krause, E., Schmitz, D., Haucke, V. Abstract: Information processing in the brain is encoded as electrical impulses in neurons that are relayed from the presynaptic compartment to postsynaptic neurons by regulated neurotransmitter release. Neurons are known to rely on autophagy for the removal of defective proteins or organelles to maintain synaptic neurotransmission and to counteract neurodegeneration. In spite of its importance for neuronal health, the physiological substrates of neuronal autophagy in the absence of proteotoxic challenge have remained largely elusive. We use knockout mice conditionally lacking the essential autophagy protein ATG5 and quantitative proteomics to demonstrate that loss of neuronal autophagy causes the selective accumulation of tubular endoplasmic reticulum (ER) in axons, resulting in increased excitatory neurotransmission and compromised postnatal viability in vivo. The gain in excitatory neurotransmission is shown to be a consequence of elevated calcium release from ER stores via ryanodine receptors accumulated in axons and at presynaptic sites. We propose a model in which neuronal autophagy controls axonal ER calcium stores to regulate neurotransmission in healthy neurons and in the brain. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.28.172460v1?rss=1 Authors: Petrucci, A. N., Joyal, K. G., Li, R., Chou, J. W., Vencer, K. M., Buchanan, G. F. Abstract: Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in patients with refractory epilepsy. A proposed risk marker for SUDEP is the duration of post-ictal generalized EEG suppression (PGES). The mechanisms underlying PGES are unknown. Serotonin (5-HT) has been implicated in SUDEP pathophysiology. Seizures suppress activity of 5-HT neurons in the dorsal raphe nucleus (DRN). We hypothesized that suppression of DRN 5-HT neuron activity contributes to PGES and increasing 5-HT neurotransmission or stimulating the DRN before a seizure would decrease PGES duration. Adult C57BL/6 and Pet1-Cre mice received EEG/EMG electrodes, a bipolar stimulating/recording electrode in the right basolateral amygdala, and either a microdialysis guide cannula or an injection of adeno-associated virus (AAV) allowing expression of channelrhodopsin2 plus an optic fiber into the DRN. Systemic application of the selective 5-HT reuptake inhibitor citalopram (20 mg/kg) decreased PGES duration from seizures induced during wake (n = 23) and NREM sleep (n = 13) whereas fluoxetine (20 mg/kg) pretreatment decreased PGES duration following seizures induced from wake (n = 11), but not NREM sleep (n = 9). Focal chemical (n = 6) or optogenetic (n = 8) stimulation of the DRN reduced PGES duration following kindled seizures and reduced morality following maximal electroshock seizures (n = 6) induced during wake. During PGES, animals exhibited immobility and suppression of EEG activity that was reduced by citalopram pretreatment. These results indicate that 5-HT and the DRN may regulate PGES and seizure-induced mortality. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.16.155077v1?rss=1 Authors: Bird, C. W., Chavez, G. J., Barber, M. J., Valenzuela, C. F. Abstract: Prenatal ethanol exposure causes a variety of cognitive deficits that have a persistent impact on quality of life, some of which may be explained by ethanol-induced alterations in interneuron function. Studies from several laboratories, including our own, have demonstrated that a single binge-like ethanol exposure during the third-trimester equivalent of human pregnancy leads to acute apoptosis and long-term loss of interneurons in the rodent retrosplenial cortex (RSC). The RSC is interconnected with the hippocampus, thalamus, and other neocortical regions and plays distinct roles in visuospatial processing and storage and retrieval of hippocampal-dependent episodic memories. Here we used slice electrophysiology to characterize the acute effects of ethanol on GABAergic neurotransmission in neonates, as well as the long-term effects of neonatal ethanol exposure on parvalbumin-interneuron mediated neurotransmission in adolescent mice. Mice were exposed to ethanol using vapor inhalation chambers. In postnatal day (P) 7 mouse pups, ethanol unexpectedly failed to potentiate GABAA receptor-mediated synaptic transmission. Binge-like ethanol exposure of P7 mice expressing channel rhodopsin in parvalbumin-positive interneurons enhanced the peak amplitudes, total charge, decays, and decreased rise-times of optically-evoked GABAA receptor-mediated inhibitory postsynaptic currents in adolescent animals. These effects could partially explain learning and memory deficits caused by developmental ethanol exposure. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.11.147439v1?rss=1 Authors: Dyer, M. S., Lewis, K. E., Walker, A. K., Dickson, T. C., Woodhouse, A., Blizzard, C. A. Abstract: Amyotrophic lateral sclerosis (ALS) is a chronic neurodegenerative disease pathologically characterised by mislocalisation of the RNA binding protein TAR-DNA binding protein 43 (TDP-43) from the nucleus to the cytoplasm. Changes to neuronal excitability and synapse dysfunction in the motor cortex are early pathological changes occurring in people with ALS and mouse models of disease. To investigate the effect of mislocalized TDP-43 on the function of motor cortex neurons we utilised mouse models that express either human wild-type (TDP-43WT) or nuclear localization sequence-deficient TDP-43 (TDP-43{Delta}NLS) on an inducible promoter that is restricted to the forebrain. Pathophysiology was investigated through immunohistochemistry and whole-cell patch-clamp electrophysiology. Thirty days expression TDP-43{Delta}NLS in adult mice (60 days of age) does not cause any changes in the number of NeuN positive nor CTIP2 positive neurons in the motor cortex. However at this time-point the expression of TDP-43{Delta}NLS drives intrinsic hyperexcitability in layer V excitatory neurons of the motor cortex. This hyperexcitability occurs concomitantly with a decrease in excitatory synaptic input to these cells. This pathophysiology is not present when TDP-43WT expression is driven, demonstrating that the localisation of TDP-43 to the cytoplasm is crucial for the altered excitability phenotype. This study has important implications for the mechanisms of toxicity of one of the most notorious proteins linked to ALS, TDP-43. We provide the first evidence that TDP-43 mislocalization causes aberrant synaptic function and a hyperexcitability phenotype in the motor cortex, linking some of the earliest dysfunctions to arise in people with ALS to mislocalisation of TDP-43. Copy rights belong to original authors. Visit the link for more info

Full Episode ► http://bit.ly/BigTreeEp1 Big Tree is a Graduate Researcher in the Li Lab at Peking University School of Life Sciences using cutting-edge neurobiology to study memory. http://yulonglilab.org CHINA

Dr. Bill Walsh is an international speaker on topics related to brain chemistry and behavior, learning, and mental health disorders. Over more than three decades as a research scientist and engineer, Dr. Walsh developed a science-based nutrient system that has helped thousands of people challenged by these disorders and is used by doctors throughout the world.His approach recognizes that nutrient imbalances can alter brain levels of key neurotransmitters, disrupt gene expression of proteins and enzymes, and cripple the body’s protection against environmental toxins.In this episode of Bulletproof Radio, we talk about Dr. Walsh’s exciting new research that includes significant developments in the areas of nutrient therapy and nutritional psychiatry, particularly Bipolar disorder. You’ll also learn the importance of the NMDA receptor and why antioxidant therapy is on its way to becoming mainstream.

Dr. Bill Walsh is an international speaker on topics related to brain chemistry and behavior, learning, and mental health disorders. Over more than three decades as a research scientist and engineer, Dr. Walsh developed a science-based nutrient system that has helped thousands of people challenged by these disorders and is used by doctors throughout the world.His approach recognizes that nutrient imbalances can alter brain levels of key neurotransmitters, disrupt gene expression of proteins and enzymes, and cripple the body’s protection against environmental toxins.In this episode of Bulletproof Radio, we talk about Dr. Walsh’s exciting new research that includes significant developments in the areas of nutrient therapy and nutritional psychiatry, particularly Bipolar disorder. You’ll also learn the importance of the NMDA receptor and why antioxidant therapy is on its way to becoming mainstream.

Dr. Randy Blakely is a Professor of Biomedical Science at Florida Atlantic University and Executive Director of the Florida Atlantic University Brain Institute. Randy lives in beautiful South Florida near the Everglades, so getting outside to enjoy nature and observe the local wildlife is a lot of fun there. He also spends his time reading, listening to audiobooks during his commutes, and listening to Americana and folk music. In the lab, Randy studies how chemicals in the brain called neurotransmitters work. He is examining how neurons control neurotransmitter signaling, as well as how medicinal drugs and drugs of abuse impact neurotransmitters and ultimately behavior. Randy received his B.A. in Philosophy from Emory University and his Ph.D. in Neuroscience from the Johns Hopkins School of Medicine. He next conducted postdoctoral research at the Yale/Howard Hughes Medical Institute Center for Molecular Neuroscience. Randy was an investigator and faculty member at Emory University and Vanderbilt university before accepting his current position at Florida Atlantic University. Randy is the recipient of numerous awards and honors for his research and mentorship. He was awarded the Daniel Efron Award from the American College of Neuropsychopharmacology, two Distinguished Investigator Awards from the Brain and Behavioral Research Foundation, a MERIT Award from the National Institute of Mental Health, a Zenith Award from the Alzheimer’s Association, the Delores C. Shockley Partnership Award in recognition of minority trainee mentorship, as well as the Astellas Award in Translational Pharmacology and the Julius Axelrod Award both from the American Society for Pharmacology and Experimental Therapeutics. In addition, he is a Fellow of the American Academy for the Advancement of Science. Randy joins us in this episode to talk more about his life and science.

Dr. Steve Mennerick is a Professor of Psychiatry and Anatomy and Neurobiology at Washington University in St. Louis. He received his PhD in Neurosciences from Washington University in St. Louis and completed a postdoctoral fellowship at the State University of New York Stony Brook. Steve has received many awards and honors during his career, including the Klingenstein Award in the Neurosciences, a NARSAD Young Investigator Award, and a Graduate Student Mentorship Award. Steve is here with us today to tell us about his journey through life and science.

Dr. Ege Kavalali is a Professor in the Departments of Physiology and Neuroscience at The University of Texas Southwestern Medical Center. He is also the Effie Marie Cain Scholar in Medical Research and the Rosewood Corporation Chair in Biomedical Science. He received his PhD in Biomedical Engineering from Rutgers University and then completed a postdoctoral fellowship at Stanford University in the department of Molecular and Cellular Physiology. Ege is with us today to tell us about his journey through life and science.

What do nerve cells look like, how do they carry information, and how does one nerve connect and communicate with another nerve? Find out in this spine-tingling Naked Science Scrapbook episode...

Die Alzheimer-Krankheit ist die häufigste Form der Demenz mit einer stetig steigenden Zahl Betroffener. Trotz intensiver Forschung sind die genauen Ursachen noch immer weitgehend ungeklärt, mit der Folge, dass bislang keine kausale Therapie zur Verfügung steht. Als einer der vermuteten Risikofaktoren gilt das Geschlecht – Frauen erkranken häufiger und mit insgesamt schwererem Verlauf an Alzheimer als Männer. Ziel der vorliegenden Studie ist es, das transgene Mausmodell Tg2576, das ein humanes Amyloid-Vorläuferprotein mit der schwedischen Doppelmutation überexprimiert, phänotypisch umfassend zu charakterisieren und auf geschlechtsspezifische Differenzen hin zu untersuchen. Dabei werden jeweils sechs männliche und sechs weibliche Träger des Transgens (Carrier) im Alter von 6, 8, 10, 12, 14 und 16 Monaten mit ihren gesunden Wurfgeschwistern (Wildtypen) verglichen. Die Tiere werden im modifizierten Hole-Board-Test über acht Tage auf kognitive, verhaltensbedingte und motorische Parameter untersucht. Ab einem Alter von 8 bis 10 Monaten weisen die Carrier im Gegensatz zu den Wildtypen progressive, signifikante Beeinträchtigungen des deklarativen Gedächtnisses und des Arbeitsgedächtnisses auf. Damit einhergehend können eine verstärkte Anwendung nicht-räumlicher Suchstrategien sowie disinhibitorische Verhaltenstendenzen beobachtet werden. Im Geschlechtervergleich sind die kognitiven Defizite der weiblichen Carrier signifikant stärker ausgeprägt. Weiterhin zeigen sich ab einem Alter von 10 Monaten geschlechtsunabhängige, progressiv fortschreitende feinmotorische Störungen beim Fressen der Belohnungsmandeln. Die Mortalität der männlichen Carrier (48,4 %) ist signifikant höher im Vergleich zu den weiblichen Carriern (25,4 %) (p = 0,005). Die weibliche Tiere weisen ein signifikant niedrigeres Gewicht als die männliche Tiere auf (p < 0,001), wobei die Carrier signifikant weniger wiegen als die Wildtypen (p < 0,001). Laboranalysen zeigen im Geschlechtervergleich einen höheren Testosterongehalt im Blutserum der männlichen Tiere und einen höheren Östradiolgehalt bei den weiblichen Tieren. Bei der Untersuchung auf mögliche zugrundeliegende Störungen der Neurotransmission können keine mit zunehmendem Alter progressiven Veränderungen der Expression spezifischer Rezeptoren (NMDAR-NR2B, mGluR5 und PBR) im Western-Blot gezeigt werden. Insgesamt erweist sich das Tg2576-Modell als ein vielversprechendes Modell der Alzheimer-Krankheit für die weitere Grundlagenforschung und präklinische Testung therapeutischer Strategien. Dabei ist es insbesondere auch für weiterführende geschlechtsspezifische Forschungsansätze geeignet.

Tue, 1 Jan 2013 12:00:00 +0100 https://epub.ub.uni-muenchen.de/23106/1/1742-2094-10-34.pdf Myint, Aye-Mu; Bogerts, Bernhard; Schwabedissen, Louise M. Zu; Bielau, Hendrik; Brisch, Ralf; Mawrin, Christian; Sarnyai, Zoltan; Bernstein, Hans-Gert; Guillemin, Gilles J.; Gos, Tomasz

Background: Immune dysfunction, including monocytosis and increased blood levels of interleukin-1, interleukin-6 and tumour necrosis factor a has been observed during acute episodes of major depression. These peripheral immune processes may be accompanied by microglial activation in subregions of the anterior cingulate cortex where depression-associated alterations of glutamatergic neurotransmission have been described. Methods: Microglial immunoreactivity of the N-methyl-D-aspartate (NMDA) glutamate receptor agonist quinolinic acid (QUIN) in the subgenual anterior cingulate cortex (sACC), anterior midcingulate cortex (aMCC) and pregenual anterior cingulate cortex (pACC) of 12 acutely depressed suicidal patients (major depressive disorder/MDD, n = 7; bipolar disorder/BD, n = 5) was analyzed using immunohistochemistry and compared with its expression in 10 healthy control subjects. Results: Depressed patients had a significantly increased density of QUIN-positive cells in the sACC (P = 0.003) and the aMCC (P = 0.015) compared to controls. In contrast, counts of QUIN-positive cells in the pACC did not differ between the groups (P = 0.558). Post-hoc tests showed that significant findings were attributed to MDD and were absent in BD. Conclusions: These results add a novel link to the immune hypothesis of depression by providing evidence for an upregulation of microglial QUIN in brain regions known to be responsive to infusion of NMDA antagonists such as ketamine. Further work in this area could lead to a greater understanding of the pathophysiology of depressive disorders and pave the way for novel NMDA receptor therapies or immune-modulating strategies.

Hirn, Mann und Testosteron Wissenschaftliche Sitzung vom 23.04.2008, Billrothhaus

In der vorliegenden Dissertation untersuchten wir mit Hilfe des psychopathologischen Tiermodells der HAB- und LAB-Ratten, welche sich nicht nur bezüglich ihrer genetisch determinierten Emotionalität und ihrer Stressbewältigungsstrategien, sondern auch hinsichtlich der Reaktivität der HPA-Achse unterscheiden, Effekte des Serotonin-Wiederaufnahmehemmers Paroxetin und von rTMS auf Verhalten und die neuroendokrine Regulation. Mit Hilfe des kombinierten DEX/CRH-Tests gelang es uns nachzuweisen, dass sich ein hohes Maß an angeborenem Angstverhalten in einer profunden Fehlregulation des Stresshormonsystems widerspiegelt. HAB-Tiere zeigten nach Verabreichung von Dexamethason einen verminderten Suppressionseffekt und die periphere Injektion von CRH führte zu einem deutlichen Anstieg der Plasmakonzentrationen von ACTH und Kortikosteron. Hierfür scheint intrahypothalamisch überexprimiertes und sezerniertes AVP verantwortlich zu sein, folglich führte auch die periphere Verabreichung eines V1-Rezeptorantagonisten zu einer Normalisierung des bei HAB-Tieren dysregulierten HPA-Systems im DEX/CRH-Test. Bindungskapazität und Bindungsaffinität von Glukokortikoid- und Mineralokortikoidrezeptoren unterschieden sich nicht zwischen den Zuchtlinien, so dass die durch Kortikosteron vermittelte Feedbackregulation des HPA-Systems auf der Ebene der intrazellulären Signalkaskade gestört zu sein scheint. Die mehrwöchige Behandlung mit dem selektiven Serotonin-Wiederaufnahmehemmer Paroxetin induzierte bei HAB-Tieren nicht nur eine durch die Verminderung der intrahypothalamischen AVP-Genexpression vermittelte Normalisierung des dysregulierten Hormonfreisetzungsprofiles im DEX/CRH-Test, sondern auch profunde Verhaltensänderungen im Forced Swim-Test, der als guter Prädiktor für die klinische Wirksamkeit einer antidepressiven Therapie angesehen wird. HAB-Tiere, welche eine passive Stressbewältigungsstrategie im Forced Swim-Test zeigen, struggelten nach Behandlung mit Paroxetin signifikant länger und verbrachten signifikant weniger Zeit mit Floating als unbehandelte HAB-Kontrolltiere. Sie waren in ihrem Verhalten von LAB-Tieren, auf die die Behandlung mit Paroxetin keinen Einfluss hatte, nicht mehr zu unterscheiden. Mit Hilfe von in vivo Mikrodialyse untersuchten wir den Einfluss von chronisch verabreichtem Paroxetin auf die stressinduzierte Freisetzung von Serotonin im dorsalen Hippocampus. Bei HAB-Tieren, welche eine angeborene verminderte Empfindlichkeit der raphé-hippocampalen Neurotransmission zeigen und den bei LAB-Tieren zu beobachtenden stressinduzierten Anstieg der Serotoninfreisetzung vermissen lassen, führte die Behandlung zu einer Normalisierung der serotonergen Neurotransmission. Dieser Effekt könnte mit der gezeigten Verminderung von SERT-Bindungsstellen im Hippocampus bei HAB- im Vergleich zu LAB-Tieren zusammenhängen, während die Expression von 5-HT1A-Rezeptoren in dieser Hirnregion unbeeinflusst blieb. Somit konnten wir erstmals zeigen, dass eine Normalisierung der Stresshormonregulation durch Paroxetin mit einem Anstieg der stressinduzierten Freisetzung von Serotonin im Hippocampus assoziiert ist. Dass rTMS der linken frontalen Hirnregionen antidepressive Effekte hat, konnte bereits in mehreren klinischen Untersuchungen an Patienten, die an Major Depression leiden, beobachtet werden. Unsere im psychopathologischen Modellorganismus der HAB/LAB-Tiere nach Langzeitbehandlung mit rTMS erzielten Ergebnisse gewähren neue Einblicke in die der antidepressiven Wirkung zugrundeliegenden neurobiologischen Mechanismen. Wie auch die Behandlung mit Paroxetin, wandelte rTMS die angeborene passive Stressbewältigungsstrategie der HAB-Tiere in eine signifikant aktivere Stressbewältigungsstragie im Forced Swim-Test um und dämpfte die endokrine Stressantwort der HPA-Achse. Die frontalen Hirnregionen partizipieren durch efferente Projektionen zum perinukleären Bereich des PVN an der Regulation der neuroendokrinen Reaktion auf Stressstimuli und kann die Synthese und Freisetzung von CRH und somit die Antwort des HPA-Systems hemmen. Wir konnten ebenfalls zeigen, dass rTMS auch während chronischem psychosozialem Stress eine dämpfende Wirkung auf die basale Aktivität der HPA-Achse hat. Allerdings ließ sich kein anregender Effekt auf die Neurogenese im Hippocampus nachweisen: rTMS erhöhte zwar leicht die Proliferationsrate hippocampaler Vorläuferzellen, verminderte jedoch die Überlebensrate BrDU-markierter Neurone. Daher scheinen andere Faktoren, neben den Glukokortikoiden, eine mindestens genauso große Rolle bei der Regulation der Anzahl und der Ausreifung der Vorläuferzellen im Hippocampus zu spielen. Wir folgern daraus, dass die Dämpfung des HPA-System wahrscheinlich ein wichtiger, der klinisch beobachteten antidepressiven Wirkung von rTMS zugrundeliegender Mechanismus ist, es mit unserem experimentellen Design jedoch nicht gelang, einen stimulierenden Effekt von rTMS auf die Neurogenese im adulten Hippocampus nachzuweisen.

Bei der kongenitalen stationären Nachtblindheit (CSNB) handelt es sich um eine klinisch und genetisch heterogene Erkrankung, die durch eine seit Geburt vorhandene nichtprogres-sive Nachtblindheit und verminderte Sehschärfe gekennzeichnet ist. Bei der x–gekoppelten Form (xlCSNB) sind zudem ein Nystagmus sowie Strabismus bei normalem Augenhinter-grund beschrieben. Aus elektrophysiologischer und psychophysischer Sicht lassen sich da-bei zwei Varianten unterscheiden. Eine Form, bei der keine Stäbchenfunktion mehr nachweisbar ist (CSNB1, komplette CSNB) sowie eine Form, bei der noch eine Reststäb-chenfunktion erhalten ist (CSNB2, inkomplette CSNB). Der Genort für die inkomplette Form war vor Beginn dieser Arbeit zwischen die Marker DXS722 und DXS255 auf Xp11.23 gekoppelt worden. Im Rahmen eines Projektes von Arbeitsgruppen aus München und Jena konnten in dieser Region zahlreiche neue Gene identifiziert werden, u. a. das CACNA1F-Gen. CACNA1F liegt auf den Cosmiden PO37 und MO111 und besteht aus 48 Exons mit einer codierenden Sequenz von 5901 Nukleotiden. Diese codieren für ein Protein von 1966 Aminsäuren Länge und einem Molekulargewicht von 219,5 kDa. Mit der Northern-Blot Hybridisierung ließ sich ausschließlich in retinalem Gewebe eine Bande nachweisen. Ver-gleichende Sequenzanalysen bestätigten die Annahme, dass CACNA1F für eine neue a 1-Untereinheit eines transvers-tubulären, spannungsabhängigen, Dihydropyridin-sensitiven Ca 2+ -Kanals vom L-Typ codiert. Aufgrund dieser Homologien und im Hinblick auf die Tatsache, dass als Pathogenese der CSNB2 eine fehlerhafte Neurotransmission vermutet wurde, wurde CACNA1F als Kandidatengen für CSNB2 in Betracht gezogen. Ziel dieser Arbeit war es, der Frage nachzugehen, ob es sich bei CACNA1F um das bei CSNB2 mutierte Krankheitsgen handelt und ob sich die vermutete genetische Heterogeni-tät von CSNB1 und CSNB2 eindeutig bestätigen lässt. Zudem sollte untersucht werden, ob es sich bei CSNB2 und der ÅIED-verwandten Form, einer Augenerkrankung, die ausge-prägte klinische und elektrophysiologische Gemeinsamkeiten mit CSNB2 aufweist, um al-lelische Erkrankungen handelt. Die Identifizierung des CACNA1F-Gens erlaubt es zudem, weitere retinale Störungen, die in dieselbe Region kartiert wurden, spezifisch auf Mutatio-nen in diesem Gen zu untersuchen, um eine Allelität auszuschließen bzw. zu bestätigen