Podcasts about ca3

Tina and Hillary cover former Kentucky politician Steve Nunn. Though a son of a former governor, Steve Nunn became a politician in his own right and had a successful career. BUT his life took a dark turn when he murdered his fiancée, shattering his future and reputation. Sources Tina's Story Herald Ledger Estate of woman slain by ex-lawmaker Steve Nunn can garnishee account containing pension payments (https://www.kentucky.com/news/politics-government/article44616372.html) NPR WKU Steve Nunn Apologizes to Ex-Fiance's Family (https://www.wkyufm.org/regional/2013-07-25/steve-nunn-apologizes-to-ex-fiances-family) State Journal ‘God will humble you,' father tells Steve Nunn (https://www.state-journal.com/news/god-will-humble-you-father-tells-steve-nunn/article_e6f97d56-d087-5c31-b8fd-3b7d53316887.html) Wikipedia [Steve Nunn](https://en.wikipedia.org/wiki/Steve_Nunn#:~:text=Stephen%20Roberts%20Nunn%20(born%20November,for%20the%20Commonwealth%20of%20Kentucky.&text=Glasgow%2C%20Kentucky%2C%20U.S.) WPSD Local 6 Kentucky Supreme Court upholds life sentence of former state representative (https://www.wpsdlocal6.com/archive/kentucky-supreme-court-upholds-life-sentence-of-former-state-representative/article_b4f4f79a-2e5f-5760-88dd-e2f44648416d.html) Photos Steve Nunn (https://bloximages.newyork1.vip.townnews.com/wpsdlocal6.com/content/tncms/assets/v3/editorial/3/54/3544fae1-b49c-59fd-9f69-3f73af56bc7f/5d40b6477f7ec.image.jpg?resize=639%2C477)--via WPSD Local 6 Nunn and Ross (https://static01.nyt.com/images/2009/11/13/us/13kentucky_CA3/popup.jpg?quality=75&auto=webp&disable=upscale)--by John Perkins via The New York Times Cemetary where Nunn was arrested (https://static01.nyt.com/images/2009/11/13/us/13kentucky_CA1/popup.jpg?quality=75&auto=webp&disable=upscale)--by Hunter Wilson via The New York Times

BUFFALO, NY- June 5, 2024 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 10, entitled, “Serine racemase expression profile in the prefrontal cortex and hippocampal subregions during aging in male and female rats.” Aging is associated with a decrease in N-methyl-D-aspartate (NMDA) receptor function, which is critical for maintaining synaptic plasticity, learning, and memory. Activation of the NMDA receptor requires binding of the neurotransmitter glutamate and also the presence of co-agonist D-serine at the glycine site. The enzymatic conversion of L-serine to D-serine is facilitated by the enzyme serine racemase (SR). Subsequently, SR plays a pivotal role in regulating NMDA receptor activity, thereby impacting synaptic plasticity and memory processes in the central nervous system. As such, age-related changes in the expression of SR could contribute to decreased NMDA receptor function. However, age-associated changes in SR expression levels in the medial and lateral prefrontal cortex (mPFC, lPFC), and in the dorsal hippocampal subfields, CA1, CA3, and dentate gyrus (DG), have not been thoroughly elucidated. In this new study, researchers Linda Bean, Prodip K. Bose, Asha Rani, and Ashok Kumar from Indiana University School of Medicine, North Florida/South Georgia Veterans Health System, and the University of Florida aimed to determine the SR expression profile, including protein levels and mRNA, for these regions in aged and young male and female Fischer-344 rats. Their results demonstrate a significant reduction in SR expression levels in the mPFC and all hippocampal subfields of aged rats compared to young rats. No sex differences were observed in the expression of SR. “These findings suggest that the decrease in SR levels may play a role in the age-associated reduction of NMDA receptor function in brain regions crucial for cognitive function and synaptic plasticity.” DOI - https://doi.org/10.18632/aging.205841 Corresponding author - Ashok Kumar - kash@ufl.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205841 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, serine racemase, hippocampus, medial prefrontal cortex (mPFC), NMDA receptor About Aging-US Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer's disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- February 15, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 3, entitled, “GV1001 reduces neurodegeneration and prolongs lifespan in 3xTg-AD mouse model through anti-aging effects.” GV1001, which mimics the activity of human telomerase reverse transcriptase, protects neural cells from amyloid beta (Aβ) toxicity and other stressors through extra-telomeric function, as noted in our prior in vitro studies. As per a recent phase II clinical trial, it improves cognitive function in patients with moderate to severe dementia. However, the underlying protective mechanisms remain unclear. In this new study, researchers Hyun-Hee Park, Hyuk Sung Kwon, Kyu-Yong Lee, Ye Eun Kim, Jeong-Woo Son, Na-Young Choi, Myung-Hoon Han, Dong Woo Park, Sangjae Kim, and Seong-Ho Koh from Hanyang University Guri Hospital, Hanyang University Graduate School of Biomedical Science and Engineering and Teloid Inc. aimed to investigate the effects of GV1001 on neurodegeneration, senescence, and survival in triple transgenic Alzheimer's disease (AD) (3xTg-AD) mice. “ [...] we hypothesised that GV1001 might have anti-aging effects and improve neurodegeneration and senescence in vivo as a possible mechanism for its beneficial effects on AD.” GV1001 (1 mg/kg) was subcutaneously injected into old 3xTg-AD mice thrice a week until the endpoint for sacrifice, and survival was analysed. Magnetic resonance imaging (MRI) and Prussian blue staining (PBS) were performed to evaluate entry of GV1001 entrance into the brain. Diverse molecular studies were performed to investigate the effect of GV1001 on neurodegeneration and cellular senescence in AD model mice, with a particular focus on BACE, amyloid beta1-42 (Aβ1-42), phosphorylated tau, volume of dentate gyrus, β-galactosidase positive cells, telomere length, telomerase activity, and ageing-associated proteins. GV1001 crossed the blood-brain barrier, as confirmed by assessing the status of ferrocenecarboxylic acid-conjugated GV1001 using magnetic resonance imaging and PBS. GV1001 increased the survival of 3xTg-AD mice. It decreased BACE and Aβ1-42 levels, neurodegeneration (i.e., reduced CA1, CA3 and dentate gyrus volume, decreased levels of senescence-associated β-galactosidase positive cells, and increased telomere length and telomerase activity), and levels of ageing-associated proteins. “We suggest that GV1001 exerts anti-ageing effects in 3xTg-AD mice by reducing neurodegeneration and senescence, which contributes to improved survival.” DOI - https://doi.org/10.18632/aging.205489 Corresponding authors - Sangjae Kim - chiron@gemvax.com, and Seong-Ho Koh - ksh213@hanyang.ac.kr Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

Technology has enhanced many aspects of business, including onboarding new employees. In Episode 104, we chat with Noel Thomas about how organisations can leverage technology to streamline onboarding tasks, improve communication, and create a more engaging experience for new hires. The impact lasts longer than the first few weeks! Noel is Co-Founder of CA3 and Eli Onboarding so he's the right person to listen too! Our conversation will help enhance your expertise and discover how you can use technology to enhance your onboarding process. Subscribe to get more episode drops, news and events https://www.theengagingemployer.com --- Send in a voice message: https://podcasters.spotify.com/pod/show/employercontentmarketing/message

Is gay retirement different? Do LGBTQ+ folks need their own retirement communities? Do some already exist and if so where?Did you know that queer people are going back into the closet as we age? That's according to an August 2023 Salon article. That's in part because of the 508 anti-LGBTQ+ laws at the state-level throughout the country, per the ACLU.That makes retirement and retirement housing more unaffordable for us - increasing the pink tax.That's why you're listening to Queer Money episode #470 because we're kicking off our new Gay Retirement 101 series.Today, we're sharing our favorite LGBTQ+ retirement communities10 of our favorite places for LGBTQ+ individuals tolive in retirement1. Pueblo Manor in Apache Junction, AZ2. Triangle Square in Hollywood, CA3. A Place for Us in Cleveland, OH4. Rainbow Vista in Gresham, OR5. Town HallApartments in Chicago, IL6. Fountaingrove Lodge in Santa Rosa, CA7. Wilton Manors, FL8. The Residences atSeashore Point in Provincetown, MA9. Village Hearth Cohousing in Durham, NC 10. Birds of a Feather in Village of Pecos, NMFor the resources and to connect with our guests, get the show notes at: https://queermoneypodcast.com/subscribe Follow us:Queer Money Instagram Queer Money YouTubeQueer Money on TiktokDownload your FREE Queer Money Kickstarter a 9-step Guide to Kickstart Your Journey to Financial Independence

In this latest episode of Stand on Guard, host David Krayden provides the lowdown of the trial of Freedom Convoy heroes Tamara Lich and Chris Barber which entered Day 28 on Monday this week. David also discusses Tamara's musical triumph last Saturday at Niagara on the Lakes and watch for a link here for a montage of Freedom Convoy protest photos that accompany Tamara's singing.KRAYDEN'S RIGHT: RESOLVE TO RESIST Thanks for watching to the end this really helps small channels like this! I include Canadian NEWS LINKS of the articles I write in my video descriptions. My Article in The Post Millennial: China infiltrated local and federal political leadership races in Canada: intelligence report: The classified document does not identify the candidate in question but only calls him "CA3." https://thepostmillennial.com/china-infiltrated-local-and-federal-political-leadership-races-in-canada-intelligence-report... SUPPORT INDEPENDENT JOURNALISM JOIN THE KRAYDEN'S RIGHT RESISTANCE: -Join YouTube Membership: https://www.youtube.com/channel/UC1ED4fuuXo07MoobImXavaQ/join -Substack FREE or Paid Subscription: https://davidkrayden.substack.com/ - Buy Me a Coffee (1 time support): https://www.buymeacoffee.com/kraydensrightSUBSCRIBE & HIT THE BELL TO KEEP SEEING THIS CHANNEL -Please SUBSCRIBE & HIT the bell. This is FREE and it will help you BEAT Trudeau's censorship so you get notifications on my YouTube Channel even when the censorship laws come into FULL effect so Trudeau and YT cannot hide this content: https://www.youtube.com/@KraydensRightwithDavidKrayden-And/or subscribe and hit the notifications on my Rumble channel to also keep informed of the latest Canadian news you won't hear on the msm https://rumble.com/user/KraydensRight... MORE ways you can find and support my work: -Krayden's Right Substack: https://davidkrayden.substack.com/ -Rumble: https://rumble.com/user/KraydensRight -Twitter: https://twitter.com/DavidKrayden -Facebook: https://www.facebook.com/KraydensRight -YouTube: https://www.youtube.com/@KraydensRightwithDavidKrayden -Apple Podcast: https://podcasts.apple.com/us/podcast/stand-on-guard-with-david-krayden/id1684148154 -Spotify Podcast: https://open.spotify.com/show/1YfyNi7gqJpRYS7iuGcWhwNEW!! You can now find Stand on Guard with David Krayden on most podcasts: Apple, Spotify, Google, Amazon, Youtube music, Substack.

David Krayden talks about how Prime Minister Justin Trudeau is blaming "MAGA" supporters of former President Donald Trump not only for the Conservative Party rejection of a free trade deal with Ukraine but for all of Trudeau's own unpopularity. Trudeau continues to demonize his political opponents as extremists when he is the real extremist.KRAYDEN'S RIGHT: RESOLVE TO RESIST Thanks for watching to the end this really helps small channels like this! I include Canadian NEWS LINKS of the articles I write in my video descriptions. My Article in The Post Millennial: China infiltrated local and federal political leadership races in Canada: intelligence report: The classified document does not identify the candidate in question but only calls him "CA3." https://thepostmillennial.com/china-infiltrated-local-and-federal-political-leadership-races-in-canada-intelligence-report... SUPPORT INDEPENDENT JOURNALISM JOIN THE KRAYDEN'S RIGHT RESISTANCE: -Join YouTube Membership: https://www.youtube.com/channel/UC1ED4fuuXo07MoobImXavaQ/join -Substack FREE or Paid Subscription: https://davidkrayden.substack.com/ - Buy Me a Coffee (1 time support): https://www.buymeacoffee.com/kraydensrightSUBSCRIBE & HIT THE BELL TO KEEP SEEING THIS CHANNEL -Please SUBSCRIBE & HIT the bell. This is FREE and it will help you BEAT Trudeau's censorship so you get notifications on my YouTube Channel even when the censorship laws come into FULL effect so Trudeau and YT cannot hide this content: https://www.youtube.com/@KraydensRightwithDavidKrayden-And/or subscribe and hit the notifications on my Rumble channel to also keep informed of the latest Canadian news you won't hear on the msm https://rumble.com/user/KraydensRight... MORE ways you can find and support my work: -Krayden's Right Substack: https://davidkrayden.substack.com/ -Rumble: https://rumble.com/user/KraydensRight -Twitter: https://twitter.com/DavidKrayden -Facebook: https://www.facebook.com/KraydensRight -YouTube: https://www.youtube.com/@KraydensRightwithDavidKrayden -Apple Podcast: https://podcasts.apple.com/us/podcast/stand-on-guard-with-david-krayden/id1684148154 -Spotify Podcast: https://open.spotify.com/show/1YfyNi7gqJpRYS7iuGcWhwNEW!! You can now find Stand on Guard with David Krayden on most podcasts: Apple, Spotify, Google, Amazon, Youtube music, Substack.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.26.550698v1?rss=1 Authors: Navacerrada, M. E. S., Kim, E., Siow, B., Ma, D., Gonzalez, L. R., Simmons, C., Hayward, D., Gibbins, D., Singh, N., Strydom, A., Fisher, E. M. C., Tybulewicz, V. L. J., Cash, D. Abstract: Down syndrome (DS) is one of the most common birth defects and the most prevalent genetic form of intellectual disability. DS arises from trisomy of chromosome 21, but its molecular and pathological consequences are not fully understood. In this study, we compared Dp1Tyb mice, a DS model, against their wild-type (WT) littermates of both sexes to investigate the impact of DS-related genetic abnormalities on the brain phenotype. We performed in vivo whole brain magnetic resonance imaging (MRI) and hippocampal 1H magnetic resonance spectroscopy (MRS) on the animals at 3 months of age. Subsequently, ex vivo MRI scans and histological analyses were conducted post-mortem. Our findings unveiled distinct neuroanatomical and biochemical alterations in the Dp1Tyb brains. Dp1Tyb brains exhibited a smaller surface area and a rounder shape compared to WT brains. Regional volumetric analysis revealed significant changes in 26 out of 72 examined brain regions, including the medial prefrontal cortex and dorsal hippocampus. These alterations were consistently observed in both in vivo and ex vivo imaging data. Additionally, high-resolution ex vivo imaging enabled us to investigate cerebellar layers and hippocampal subregions, revealing selective areas of decrease and remodelling in these structures. An analysis of hippocampal metabolites revealed an elevation in glutamine and the glutamine/glutamate ratio in the Dp1Tyb mice compared to controls, suggesting a possible imbalance in the excitation/inhibition ratio. This was accompanied by the decreased levels of taurine. Histological analysis revealed fewer neurons in the hippocampal CA3 and DG layers, along with an increase in astrocytes and microglia. These findings recapitulate multiple neuroanatomical and biochemical features associated with DS, enriching our understanding of the potential connection between chromosome 21 trisomy and the resultant phenotype. 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/2023.07.16.549236v1?rss=1 Authors: Tan, J., Xu, H., Liao, G.-y., An, J. J., Xu, B. Abstract: At the center of the hippocampal tri-synaptic loop are synapses formed between mossy fiber (MF) terminals from granule cells in the dentate gyrus (DG) and proximal dendrites of CA3 pyramidal neurons. However, the molecular mechanism regulating the development and function of these synapses is poorly understood. In this study, we showed that neurotrophin-3 (NT3) was expressed in nearly all mature granule cells but not CA3 cells. We selectively deleted the NT3-encoding Ntf3 gene in the DG during the 1st two postnatal weeks to generate a Ntf3 conditional knockout (Ntf3-cKO). Ntf3-cKO mice had normal hippocampal cytoarchitecture but displayed elevated anxiety level and impairments in contextual memory, spatial reference memory and nest building. As MF-CA3 synapses are essential for encoding of contextual memory, we examined synaptic transmission at these synapses using ex vivo electrophysiological recordings. We found that Ntf3-cKO mice showed impaired basal synaptic transmission due to deficits in excitatory postsynaptic currents mediated by AMPA receptors but normal presynaptic function and intrinsic excitability of CA3 pyramidal neurons. Consistent with this selective postsynaptic deficit, Ntf3-cKO mice had fewer and smaller thorny excrescences on proximal apical dendrites of CA3 neurons and lower GluR1 levels in the stratum lucidum area where MF-CA3 synapses reside but normal MF terminals, compared with control mice. Thus, our study indicates that NT3 expressed in the dentate gyrus is crucial for the postsynaptic structure and function of MF-CA3 synapses and hippocampal-dependent memory. 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/2023.07.03.547282v1?rss=1 Authors: Bjornson, K. J., Vanderplow, A. M., Yang, Y., Kermath, B. A., Cahill, M. E. E. Abstract: The effects of repeated stress on cognitive impairment are thought to be mediated, at least in part, by reductions in the stability of dendritic spines in brain regions critical for proper learning and memory, including the hippocampus. Small GTPases are particularly potent regulators of dendritic spine formation, stability, and morphology in hippocampal neurons. Through the use of small GTPase protein profiling in mice, we identify increased levels of synaptic Rap1 in the hippocampal CA3 region in response to escalating, intermittent stress. We then demonstrate that increased Rap1 in the CA3 is sufficient in and of itself to produce stress-relevant dendritic spine and cognitive phenotypes. Further, using super-resolution imaging, we investigate how the pattern of Rap1 trafficking to synapses likely underlies its effects on the stability of select dendritic spine subtypes. These findings illuminate the involvement of aberrant Rap1 regulation in the hippocampus in contributing to the psychobiological effects of stress. 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/2023.06.21.546025v1?rss=1 Authors: Sauvage, M. M., Ku, S.-P., Atucha, E., Alavi, N., Yoshida, M., Csicsvari, J. Abstract: How the coordination of neuronal spiking activity and brain rhythms between hippocampal subregions supports memory function remains elusive. We studied interregional coordination of CA3 neuronal spiking activity with CA1 theta oscillations by recording electrophysiological signals along the proximodistal axis of the hippocampus in rats performing a high memory demand recognition memory task adapted from humans. We found that CA3 population spiking activity occurs preferentially at the peak of distal CA1 theta oscillations only when animals recalled previously encountered stimuli. In addition, decoding analyses revealed that only population cell firing of proximal CA3 together with that of distal CA1 can predict memory performance in the present non-spatial task. Overall, our work demonstrates an important role of the synchronization of CA3 neuronal activity with CA1 theta oscillations for successful recognition memory. 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/2023.03.29.534692v1?rss=1 Authors: Eom, K., Kim, Y., Baek, S., Park, A. J., Ho, W.-K., Lee, S.-H. Abstract: Neuronal excitability is a key determinant for recruitment of a neuron to an ensemble. High-frequency mossy fiber (MF) inputs induce prolonged increases in the excitability of a CA3 pyramidal cell (long-term potentiation of intrinsic excitability, LTP-IE), which primes the cell such that weak perforant pathway (PP) inputs can induce long-term potentiation at PP synapses (PP-LTP). However, sustained hyperexcitability can be detrimental, and a mechanism to reverse this state is necessary. Here, we show that burst firings of CA3 pyramidal cells elicited by PP or recurrent inputs reverse the MF-induced LTP-IE. Moreover, the high-frequency PP inputs to CA3-PCs already primed by MF inputs induced not only PP-LTP but also restored the high excitability state. Labeling neuronal ensemble using c-fos promoter in animals exposed to a novel context, we found most CA3 ensemble cells exhibited increased excitability, indicative of LTP-IE. Moreover, when the animals experienced novel contexts twice with a 30 min interval, a substantial subset of putative twice-activated CA3 ensemble cells exhibited reduced excitability, implying depotentiation of LTP-IE. We developed an in silico model based on the experimental results and found that MF-induced LTP-IE and its depotentiation are critical for the association of neuronal ensembles representing temporally spaced events. 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/2023.03.28.534509v1?rss=1 Authors: El-Oussini, H., Zhang, C.-L., Francois, U., Castelli, C., Lampin Saint-Amaux, A., Lepleux, M., Molle, P., Velez, L., Dejean, C., Lanore, F., Herry, C., Choquet, D., Humeau, Y. Abstract: Consolidation of recent memory depends on hippocampal activities during resting periods that immediately follows the memory encoding. There, Slow Save Sleep phases appear as privileged periods for memory consolidation as hosting the ripple activities, which are fast oscillations generated within the hippocampus whose inactivation leads to memory impairment. If a strong correlation exists between these replays of recent experience and the persistence of behavioural adaptations, the mobilisation, the localization and the importance of synaptic plasticity events in this process is largely unknown. To question this issue, we used cell-surface AMPAR immobilisation to block post-synaptic LTP within the hippocampal region at various steps of the memory process. 1- Our results show that hippocampal synaptic plasticity is engaged during the consolidation but is dispensable during the encoding or recall of a working memory based spatial memory task. 2- Blockade of plasticity during sleep leads to apparent forgetting of the encoded rule. 3- In vivo recordings of ripple activities during resting periods show a strong impact of AMPAR immobilization solely, prominent when a rule has been recently encoded. 4- In situ examination of the interplay between AMPAR mobility, hippocampal plasticity and spontaneous ripple activities pointed that post-synaptic plasticity at CA3-CA3 recurrent synapses support ripple generation. As crucial results were reproduced using another AMPARM blockade strategy, we propose that after rule encoding, post-synaptic AMPAR mobility at CA3 recurrent synapses support the generation of ripples necessary for rule consolidation. 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/2023.03.14.532607v1?rss=1 Authors: Miranda, M., Silva, A., Morici, J. F., Coletti, M. A., Belluscio, M., Bekinschtein, P. Abstract: In a constantly changing environment, organisms face the challenge of adapting their behavior by retrieving previous experiences or acquiring new information. Previous research has postulated that this balance between memory generalization and differentiation manifests in a dichotomic manner. When environmental information exceeds a given threshold, activation of a stored representation could initiate retrieval, but below this threshold, a novel event could be encoded with a concomitant remapping of the internal representation in the hippocampus. Here, we examined the hippocampal molecular and neuronal mechanisms underlying retrieval in a cue-degraded environment by combining in vivo electrophysiological recordings and pharmacological manipulations. We developed a memory recognition task that allows a graded decrease in the contextual cues present during retrieval. We found that the manipulation of the number of visual cues was consistent with the activation or not of the contextual memory trace. Retrieval of a specific context memory was reflected by the level of CA3 remapping, demonstrating a clear relationship between remapping and contextual recognition. Also, manipulation of NMDAR activity in the DG-CA3 circuit bidirectionally modulated contextual memory retrieval. The blockade of NMDAR in CA3 impaired recognition in a cue-degraded, but not in a full-cue context, while their activation has the opposite effect. Conversely, blockade of NMDAR in the DG promoted retrieval under an even more cue-degraded environment, while activation had the opposite effect. Our results provide evidence for a flexible interaction between environmental cues and information stored in the hippocampus and give new insights into the biological mechanisms that balance memory encoding and retrieval. 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/2023.02.21.529365v1?rss=1 Authors: Kang, L., Toyoizumi, T. Abstract: The hippocampal subfield CA3 is thought to function as an autoassociative network that stores sensory information as memories. This information arrives via the entorhinal cortex (EC), which projects to CA3 directly as well as indirectly through the dentate gyrus (DG). DG sparsifies and decorrelates the information before also projecting to CA3. The computational purpose for receiving two encodings of the same sensory information has not been firmly established. We model CA3 as a Hopfield-like network that stores both correlated and decorrelated encodings and retrieves them at low and high inhibitory tone, respectively. As more memories are stored, the dense, correlated encodings merge along shared features while the sparse, decorrelated encodings remain distinct. In this way, the model learns to transition between concept and example representations by controlling inhibitory tone. To experimentally test for the presence of these complementary encodings, we analyze the theta-modulated tuning of phase-precessing place cells in rat CA3. In accordance with our model's prediction, these neurons exhibit more precise spatial tuning and encode more detailed task features during theta phases with sparser activity. Finally, we generalize the model beyond hippocampal architecture and find that feedforward neural networks trained in multitask learning benefit from a novel loss term that promotes hybrid encoding using correlated and decorrelated representations. Thus, the complementary encodings that we have found in CA3 can provide broad computational advantages for solving complex tasks. 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/2023.02.18.529095v1?rss=1 Authors: Hernandez, A. R., Barrett, M. E., Lubke, K. N., Maurer, A., Burke, S. N. Abstract: Age-related cognitive decline has been linked to distinct patterns of cellular dysfunction in the prelimbic cortex (PL) and the CA3 subregion of the hippocampus. Because higher cognitive functions require both structures, selectively targeting a neurobiological change in one region, at the expense of the other, is not likely to restore normal behavior in older animals. One change with age that both the PL and CA3 share, however, is a reduced ability to utilize glucose, which can produce aberrant neural activity patterns. The current study used a ketogenic diet (KD) intervention, which reduces the brain's reliance on glucose, and has been shown to improve cognition, as a metabolic treatment for restoring neural ensemble dynamics in aged rats. Expression of the immediate-early genes Arc and Homer1a were used to quantify the neural ensembles that were active in the home cage prior to behavior, during a working memory/biconditional association task, and a continuous spatial alternation task. Aged rats on the control diet had increased activity in CA3 and less ensemble overlap in PL between different task conditions than did the young animals. In the PL, the KD was associated with increased activation of neurons in the superficial cortical layers. The KD did not lead to any significant changes in CA3 activity. These observations suggest that the KD does not restore neuron activation patterns in aged animals, but rather the availability of ketone bodies in the frontal cortices may permit the engagement of compensatory mechanisms that produce better cognitive outcomes. 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/2023.02.15.528683v1?rss=1 Authors: Soula, M., Maslarova, A., Harvey, R. E., Valero, M., Brandner, S., Hamer, H., Fernandez Ruiz, A., Buzsaki, G. Abstract: Interictal epileptiform discharges (IEDs) are transient abnormal electrophysiological events commonly observed in epilepsy patients but are also present in other neurological disease, such as Alzheimer's disease (AD). Understanding the role IEDs have on the hippocampal circuit is important for our understanding of the cognitive deficits seen in epilepsy and AD. We characterize and compare the IEDs of human epilepsy patients from microwire hippocampal recording with those of AD transgenic mice with implanted multi-layer hippocampal silicon probes. Both the local field potential features and firing patterns of pyramidal cells and interneurons were similar in mouse and human. We found that as IEDs emerged from the CA3-1 circuits, they recruited pyramidal cells and silenced interneurons, followed by post-IED suppression. IEDs suppressed the incidence and altered the properties of physiological sharp-wave ripples (SPW-Rs), altered their physiological properties, and interfered with the replay of place field sequences in a maze. In addition, IEDs in AD mice inversely correlated with daily memory performance. Together, our work implicates that IEDs may present a common and epilepsy-independent phenomenon in neurodegenerative diseases that perturbs hippocampal-cortical communication and interferes with memory. 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/2023.02.05.527133v1?rss=1 Authors: Yiu, Y.-H., Leibold, C. Abstract: Hippocampal place cell sequences have been hypothesized to serve as diverse purposes as the induction of synaptic plasticity, formation and consolidation of long-term memories, or navigation and planning. The interrelation of sequence replay during offline states such as sleep or consummatory behaviors and online theta sequences during running and navigation is highly debated. Offline sequences are inherently 1-dimensional, whereas online sequences reverse with running direction and thus reflect the 2-dimensional topology of space, which poses a fundamental and unresolved inconsistency. Here, we propose a computational model of cornu ammonis 3 (CA3) and dentate gyrus (DG), where sensorimotor input drives the direction-dependent online sequences within CA3, and the intrahippocampal CA3-DG projections produces prospective intrinsic sequences. The model thereby suggests that sequence propagation on multiple 1-D manifolds underlies a relational code that contains stable signatures for the encoding of spatial memories and that could be used for prospective planning. 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/2023.02.01.526349v1?rss=1 Authors: Harbin, N. H., Lustberg, D. J., Hurst, C., Pare, J.-F., Crotty, K. M., Waters, A. L., Yeligar, S. M., Smith, Y., Seyfried, N. T., Weinshenker, D., Hepler, J. R. Abstract: RGS14 is a complex multifunctional scaffolding protein that is highly enriched within pyramidal cells (PCs) of hippocampal area CA2. There, RGS14 suppresses glutamate-induced calcium influx and related G protein and ERK signaling in dendritic spines to restrain postsynaptic signaling and plasticity. Previous findings show that, unlike PCs of hippocampal areas CA1 and CA3, CA2 PCs are resistant to a number of neurological insults, including degeneration caused by temporal lobe epilepsy (TLE). While RGS14 is protective against peripheral injury, similar roles for RGS14 during pathological injury in hippocampus remain unexplored. Recent studies show that area CA2 modulates hippocampal excitability, generates epileptiform activity and promotes hippocampal pathology in animal models and patients with TLE. Because RGS14 suppresses CA2 excitability and signaling, we hypothesized that RGS14 would moderate seizure behavior and early hippocampal pathology following seizure activity. Using kainic acid (KA) to induce status epilepticus (KA-SE) in mice, we show loss of RGS14 (RGS14 KO) accelerated onset of limbic motor seizures and mortality compared to wild type (WT) mice, and that KA-SE upregulated RGS14 protein expression in CA2 and CA1 PCs of WT. Utilizing proteomics, we saw loss of RGS14 impacted the expression of a number of proteins at baseline and after KA-SE, many of which associated unexpectedly with mitochondrial function and oxidative stress. RGS14 was shown to localize to the mitochondria in CA2 PCs of mice and reduce mitochondrial respiration in vitro. As a readout of oxidative stress, we found RGS14 KO dramatically increased 3-nitrotyrosine levels in CA2 PCs, which was greatly exacerbated following KA-SE and correlated with a lack of superoxide dismutase 2 (SOD2) induction. Assessing for hallmarks of seizure pathology in RGS14 KO, we observed worse neuronal injury in area CA3 (but none in CA2 or CA1), and a lack of microgliosis in CA1 and CA2 compared to WT. Together, our data demonstrates a newly appreciated neuroprotective role for RGS14 against intense seizure activity in hippocampus. Our findings are consistent with a model where, after seizure, RGS14 is upregulated to support mitochondrial function and prevent oxidative stress in CA2 PCs, limit seizure onset and hippocampal neuronal injury, and promote microglial activation in hippocampus. 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/2023.02.03.526955v1?rss=1 Authors: Sahay, A., Shi, Y.-T., Alipio, J. B. Abstract: Heterozygous mutations in the Dual specificity tyrosine-phosphorylation-regulated kinase 1a Dyrk1a gene define a syndromic form of Autism Spectrum Disorder. The synaptic and circuit mechanisms mediating Dyrk1a functions in social cognition are unclear. Here, we identify a social experience-sensitive mechanism in hippocampal mossy fiber-parvalbumin interneuron (PV IN) synapses by which Dyrk1a recruits feed-forward inhibition of CA3 and CA2 to promote social recognition. We employ genetic epistasis logic to identify a cytoskeletal protein, Ablim3, as a synaptic substrate of Dyrk1a. We demonstrate that Ablim3 downregulation in dentate granule cells of adult hemizygous Dyrk1a mice is sufficient to restore PV IN mediated inhibition of CA3 and CA2 and social recognition. Acute chemogenetic activation of PV INs in CA3/CA2 of adult hemizygous Dyrk1a mice also rescued social recognition. Together, these findings illustrate how targeting Dyrk1a synaptic and circuit substrates as enhancers of Dyrk1a function harbors potential to reverse Dyrk1a haploinsufficiency-associated circuit and cognition impairments. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Even though Steelers receiver Calvin Austin III didn't play in 2022, it doesn't mean that the rookie didn't get acclimated to the Steeler Way last year. Join Bryan Anthony Davis for an exclusive interview with the man known as CA3. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.26.525630v1?rss=1 Authors: Caron, D., Buccelli, S., Canal-Alonso, A., Hernandez, M., Pruzzo, G., Corchado, J. M., Chiappalone, M., Panuccio, G. Abstract: Hippocampal dysfunction is the hallmark of mesial temporal lobe epilepsy (MTLE), the most common epileptic syndrome in adults and the most often refractory to medical therapy. Deep brain stimulation (DBS) may ameliorate drug-refractory MTLE, but it still cannot guarantee a seizure-free life. One major drawback is that the stimulation policy is informed by trial-and-error rather than by the operating mode of the brain. Thus, optimizing DBS parameters is still an unmet clinical need. Here, we propose the deployment of hippocampal interictal activity in a biohybrid approach to control limbic ictogenesis. Specifically, an electronic bridge establishes a graft-host interaction between the hippocampal subfield CA3 (graft) and the parahippocampal cortex (CTX - host) of distinct rodent brain slices, both treated with 4-aminopyridine; the electronic bridge relays the graft interictal events to the host via electrical pulses. We show that interictal activity generated by the graft CA3 controls limbic ictogenesis in the host CTX even in the absence of feedback from it, thus likely reflecting an intrinsic anti-ictogenic clock of this brain region. This work opens a translational perspective for MTLE treatment via biohybrid neuroprostheses relying on the intrinsic clock of incorporated hippocampal cells. 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/2023.01.26.525627v1?rss=1 Authors: Caron, D., Buccelli, S., Canal-Alonso, A., Puthanmadam Subramaniyam, N., Farsani, J., Pruzzo, G., Linares Barranco, B., Hyttinen, J., Corchado, J. M., Chiappalone, M., Panuccio, G. Abstract: Objective. The compromise of the hippocampal loop is a hallmark of mesial temporal lobe epilepsy (MTLE); particularly, the hippocampal output to the parahippocampal cortex is disrupted by damage of the CA1. While closed-loop deep brain stimulation (DBS) is the latest frontier to improve drug-refractory MTLE, current approaches do not restore the hippocampal loop, are designed by trial-and-error and heavily rely on seizure detection or prediction algorithms. The objective of this study is to evaluate the efficacy and robustness of bridging hippocampus and cortex via closed-loop stimulation to achieve the functional restoration of the hippocampal loop and control limbic seizures. Approach. In hippocampus-cortex slices treated with 4-aminopyridine and in which the Schaffer Collaterals are severed, we used interictal discharges originating in the CA3 to trigger stimulation in the subiculum and re-establish the hippocampus output to the cortex. Combining tools from information theory with quantification of ictal activity, we addressed the efficacy of the bridge in restoring the functional connectivity of the hippocampal loop and controlling ictogenesis. Main results. Bridging hippocampus and cortex recovered the functional connectivity of the hippocampal loop, controlled ictogenesis and proved robust to failure mimicking the functional impairment of the CA3 seen in MTLE rodent models and patients. The efficacy and robustness of the bridge stem in mirroring the adaptive properties of the CA3, which acts as biological neuromodulator. Significance. A DBS device that does not depend on seizure detection/prediction algorithms but relies on endogenous interictal patterns presents the key to advance the conceptual design of current DBS paradigms for epilepsy treatment. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

This week it's just us...again.Shout out @yourtipsyhomegirl follow her on ig and tiktok Book her for your next event or learn how to make specialty cocktails one on one For all promo codes and links for promotions in the episode, follow this link:https://linktr.ee/cocktalesadsFollow Us!@cocktalespodcast@kikisaidso@coffeebeandeanContact Us:Advice: advice@cocktalespod.comCocktales: cocktales@cocktalespod.comTour Sponsorship: sales@cocktalespod.comIn show advertising: camila@pleasurepodcasts.comGet Your Merch & Order Your Card Gamewww.imcurioustoknow.comGet Klassy Bastewww.klassybaste.comTravel with Medinah!https://paradiseandvibe.com/Live Show Tix (All Cities) Tickets on Sale NowDirty Little Secrets Tour 2023www.linktr.ee/cocktalespodcast1/26: Charleston, SC2/23: Los Angeles, CA3/2: Nashville, TN3/9: Orlando, FL3/16: Miami, FL3/24: Pontiac, MI 4/8: Seattle, WA4/15: Toronto, ON5/11: Birmingham, AL **Just added On Sale 1/24 for Patreon5/20: Dallas, TXLinks to tickets here: www.linktr.ee/cocktalespodcast

This week it's just us! Cocktail of the week:The Mean One2 oz. Tequila 1 oz. Melon Liqueur0.5 oz. Lime Juice0.5 oz. Simple SyrupInstructions:Rim the glass with lime juice and coat rim with red sugarRefrigerate glass for a few minutes to let sugar set.Add Tequila, Melon Liqueur , Lime Juice & Simple Syrup into a cocktail shaker filled with iceShake for 5-10 seconds.pour from the shaker over ice. Garnish with a mini candy cane & Enjoy!Shout out @yourtipsyhomegirl follow her on ig and tiktok Book her for your next event or learn how to make specialty cocktails one on one For all promo codes and links for promotions in the episode, follow this link:https://linktr.ee/cocktalesadsFollow Us!@cocktalespodcast@kikisaidso@coffeebeandeanGet Your Merch & Order Your Card Gamewww.imcurioustoknow.comGet Klassy Bastewww.klassybaste.comTravel with Medinah!https://paradiseandvibe.com/Live Show Tix (All Cities) Tickets on Sale NowDirty Little Secrets Tour 2023www.linktr.ee/cocktalespodcast1/26: Charleston, SC2/23: Los Angeles, CA3/2: Nashville, TN3/9: Orlando, FL3/16: Miami, FL3/24: Pontiac, MI 4/8: Seattle, WA4/15: Toronto, ON5/11: Birmingham, AL **Just added On Sale 1/24 for Patreon5/20: Dallas, TXLinks to tickets here: www.linktr.ee/cocktalespodcast

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.16.520658v1?rss=1 Authors: Chang, H., Esteves, I. M., Neumann, A. R., Mohajerani, M. H., McNaughton, B. L. Abstract: Episodic memory depends on the association of diverse attribute representations that are distributed across the neocortex, and evidence suggests that these attributes are linked, at least initially, by the hippocampus, which orchestrates retrieval and the offline replay of experience during memory consolidation. The dynamics that characterize this hippocampal-cortical dialogue, however, are only partly understood. Although it was originally proposed that replay is initiated in CA3, with the spontaneous emission of sharp-wave ripple (SWR) bursts, increasing evidence suggests that cortex may seed the process with partial information, leading to pattern completion in CA3 and subsequent global reactivation of the episode. A recent study has shown that the secondary motor cortex (M2), among other areas, carries two distinct types of representations: place cell-like activity, which relies on an intact hippocampus for its development, and responses tied to visuo-tactile cues -- the 'attributes' of the experience, which do not require the hippocampus. Using two-photon Ca2+ imaging, while simultaneously acquiring LFP from the ipsilateral CA1, we assessed the interactions among cortical retrieval of visuo-tactile attributes of previous experiences in a virtual environment, hippocampal SWR, and the cortical reinstatement of the spatial aspects of the same experiences. During rest after the experience, two types of reactivation events occurred, which separately conveyed information about spatial trajectories and visuo-tactile attributes. Reactivation of attribute information preceded that of trajectories in relation to hippocampal SWRs. Furthermore, paired reactivations of cue and trajectory information supported similar features of previous experiences. These results are consistent with the hypothesis that cortical retrieval of non-spatial attributes of recent experience seeds hippocampal reactivation of associated spatial sequences, which is followed by retrieval of episodic memory traces. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

This week we're joined by comedian K Dubb @comediankdubb23Cocktail of the week:Sticky-ickyPunch Bowl Measurement:1/2 of a 750 ml Bottle of Caramel Vodka1 Bottle of Moscato1/2 Gallon of Apple CiderClub SodaApple Slices Instructions:Add Caramel Vodka, Moscato, and Apple Cider into a Punch bowl.Stir and add in your apple slices to your punch bowl.Refrigerate for a couple hours.When you're ready to serve, pour over ice and top with club soda. Garnish with some apple slices and a cinnamon stick & Enjoy!For all promo codes and links for promotions in the episode, follow this link:https://linktr.ee/cocktalesadsFollow Us!@cocktalespodcast@kikisaidso@coffeebeandeanGet Your Merch & Order Your Card Gamewww.imcurioustoknow.comGet Klassy Bastewww.klassybaste.comLive Show Tix (All Cities) Tickets on Sale NowDirty Little Secrets Tour 2023www.linktr.ee/cocktalespodcast1/26: Charleston, SC2/23: Los Angeles, CA3/2: Nashville, TN3/9: Orlando, FL3/16: Miami, FL3/24: Pontiac, MI 4/8: Seattle, WA4/15: Toronto, ON5/11: Birmingham, AL **Just added5/20: Dallas, TXLinks to tickets here: www.linktr.ee/cocktalespodcast

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.14.520457v1?rss=1 Authors: Hoffman, J. L., Faccidomo, S., Taylor, S. M., DeMiceli, K. G., May, A. M., Smith, E. N., Whindleton, C. M., Hodge, C. W. Abstract: Rationale: The development and progression of alcohol use disorder (AUD) is widely viewed as maladaptive neuroplasticity. The transmembrane alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) regulatory protein 8 (TARP {gamma}-8) is a molecular mechanism of neuroplasticity that has not been evaluated in AUD or other addictions. Objective: To address this gap in knowledge, we evaluated the mechanistic role of TARP {gamma}-8 bound AMPAR activity in the basolateral amygdala (BLA) and ventral CA3 hippocampus (vHPC) in the positive reinforcing effects of alcohol, which drive repetitive alcohol use throughout the course of AUD, in C57BL/6J mice. These brain regions were selected because they exhibit high levels of TARP {gamma}-8 expression and send glutamate projections to the nucleus accumbens (NAc), which is a key nucleus in the brain reward pathway. Methods and Results: Site-specific pharmacological inhibition of AMPARs bound to TARP {gamma}-8 in the BLA via bilateral infusion of the selective negative modulator JNJ-55511118 significantly decreased operant alcohol self-administration with no effect on sucrose self-administration in behavior-matched controls. Temporal analysis showed that reduction of alcohol-reinforced responding occurred greater than 25 min after the onset of responding, consistent with a blunting of the positive reinforcing effects of alcohol in the absence of nonspecific behavioral effects. In contrast, inhibition of TARP {gamma}-8 bound AMPARs in the vHPC selectively decreased sucrose self-administration with no effect on alcohol. Conclusions: This study reveals a novel brain region-specific role of TARP {gamma}-8 bound AMPARs as a molecular mechanism of the positive reinforcing effects of alcohol and non-drug rewards. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

This week we finally have a little time to sip slow, catch our breath and catch up!For all promo codes and links for promotions in the episode, follow this link:https://linktr.ee/cocktalesadsFollow Us!@cocktalespodcast@kikisaidso@coffeebeandeanDownload Amorus today for delicious sexy games with your partner www.amorus.net/cocktalesGet Your Merch & Order Your Card Gamewww.imcurioustoknow.comGet Klassy Bastewww.klassybaste.comPlease support this film project by Carlos Avileshttps://seedandspark.com/fund/rainbowsun#storyLive Show Tix (All Cities) Tickets on Sale Now12/10 Houston, TXDirty Little Secrets Tour 2023www.linktr.ee/cocktalespodcast1/26: Charleston, SC2/23: Los Angeles, CA3/2: Nashville, TN3/9: Orlando, FL3/16: Miami, FL3/24: Pontiac, MI 4/8: Seattle, WA4/15: Toronto, ON5/11: Birmingham, AL **Just added5/20: Dallas, TXLinks to tickets here: www.linktr.ee/cocktalespodcast

This week we're joined by singer/songwriter Vedo! We're talking about what inspires a writer to make songs about you, splitting time with families for Christmas, spitting in mouths, and cheating.Check out our guest Vedo on all social media platforms and Youtube he's @vedothesingerNew EP “While You Wait” with OG ParkerAlbum drops Dec 2nd!For all promo codes and links for promotions in the episode, follow this link:https://linktr.ee/cocktalesadsFollow Us!@cocktalespodcast@kikisaidso@coffeebeandeanDownload Amorus today for delicious sexy games with your partner www.amorus.net/cocktalesGet Your Merch & Order Your Card Gamewww.imcurioustoknow.comGet Klassy Bastewww.klassybaste.comPlease support this film project by Carlos Avileshttps://seedandspark.com/fund/rainbowsun#storyLive Show Tix (All Cities) Tickets on Sale Now12/10 Houston, TXDirty Little Secrets Tour 2023www.linktr.ee/cocktalespodcast1/26: Charleston, SC2/23: Los Angeles, CA3/2: Nashville, TN3/9: Orlando, FL3/16: Miami, FL3/24: Pontiac, MI 4/8: Seattle, WA4/15: Toronto, ON5/20: Dallas, TXLinks to tickets here: www.linktr.ee/cocktalespodcast

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.29.518458v1?rss=1 Authors: Lee, C., Lee, B. H., Jung, H., Lee, C., Sung, Y., Kim, H., Kim, J., Shim, J. Y., Kim, J.-i., Choi, D. I., Park, H. Y., Kaang, B.-K. Abstract: As basic units of neural networks, ensembles of synapses underlie cognitive functions like learning and memory. These synaptic engrams show elevated synaptic density among engram cells following contextual fear memory formation. Subsequent analysis of the CA3-CA1 engram synapse revealed larger spine sizes, as the synaptic connectivity correlated to the memory strength. Here, we elucidate the synapse dynamics between CA3 and CA1 by tracking identical synapses at multiple time points by adapting two-photon microscopy and dual-eGRASP technique in vivo. After memory formation, synaptic connections between engram populations are enhanced in conjunction with synaptogenesis within the hippocampal network. However, extinction learning specifically correlated with the disappearance of CA3 engram to CA1 engram (E-E) synapses. We observed newly formed synapses near pre-existing synapses, which clustered CA3-CA1 engram synapses after fear memory formation. Overall, we conclude that dynamics at CA3 to CA1 E-E synapses are key sites for modification during fear memory states. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

This week we're joined by Karlous Miller of 85 South and we're talking about why men fix their cars after a breakup, who needs their kitty repossessed, and what to do when you find yourself in a fishy situation.For all promo codes and links for promotions in the episode, follow this link:https://linktr.ee/cocktalesadsFollow Us!@cocktalespodcast@kikisaidso@coffeebeandeanDownload Amorus today for delicious sexy games with your partner www.amorus.net/cocktalesGet Your Merch & Order Your Card Gamewww.imcurioustoknow.comGet Klassy Bastewww.klassybaste.comPlease support this film project by Carlos Avileshttps://seedandspark.com/fund/rainbowsun#storyLive Show Tix (All Cities) Tickets on Sale Now12/10 Houston, TXDirty Little Secrets Tour 2023www.linktr.ee/cocktalespodcast1/26: Charleston, SC2/23: Los Angeles, CA3/2: Nashville, TN3/9: Orlando, FL3/16: Miami, FL3/24: Pontiac, MI 4/8: Seattle, WA4/15: Toronto, ON5/20: Dallas, TXLinks to tickets here: www.linktr.ee/cocktalespodcast

Have you ever given a presentation of all your past relationships with your current significant other? For all promo codes and links for promotions in the episode, follow this link:https://linktr.ee/cocktalesadsFollow Us!@cocktalespodcast@kikisaidso@coffeebeandeanDownload Amorus today for delicious sexy games with your partner www.amorus.net/cocktalesGet Your Merch & Order Your Card Gamewww.imcurioustoknow.comGet Klassy Bastewww.klassybaste.comPlease support this film project by Carlos Avileshttps://seedandspark.com/fund/rainbowsun#storywww.Squirtopia.com - follow them on Instagram @squirtopia use code: COCKTALES for 10% off the SquirtPadLive Show Tix (All Cities) Tickets on Sale 11/18/2212/10 Houston, TXDirty Little Secrets Tour 2023www.linktr.ee/cocktalespodcast1/26: Charleston, SC2/23: Los Angeles, CA3/2: Nashville, TN3/9: Orlando, FL3/16: Miami, FL3/24: Pontiac, MI 4/8: Seattle, WA4/15: Toronto, ON5/20: Dallas, TXLinks to tickets here: www.linktr.ee/cocktalespodcast

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.09.515872v1?rss=1 Authors: Whitebirch, A. C., Barnett, A., Santoro, B., Scharfman, H. E., Siegelbaum, S. A. Abstract: A significant proportion of temporal lobe epilepsy (TLE) patients experience drug-resistant seizures associated with mesial temporal sclerosis, in which there is extensive cell loss in the hippocampal CA1 and CA3 subfields, with a relative sparing of dentate gyrus granule cells and the CA2 pyramidal neurons. A role for CA2 in seizure generation was suggested based on findings of a reduction in synaptic inhibition (Williamson & Spencer, 1994) and the presence of interictal-like spike activity in resected hippocampal tissue from TLE patients (Wittner et al., 2009). We recently found that in the pilocarpine-induced status epilepticus mouse model of TLE there was an increase in CA2 intrinsic excitability associated with a loss of CA2 synaptic inhibition. Furthermore, chemogenetic silencing of CA2 significantly reduced seizure frequency, consistent with a role of CA2 in promoting seizure generation and/or propagation (Whitebirch et al., 2022). In the present study we explored the basis of this inhibitory deficit using immunohistochemical and electrophysiological approaches. We report a widespread decrease in the density of pro-cholecystokinin-immunopositive interneurons and a functional impairment of cholecystokinin-expressing interneuron-mediated inhibition of CA2 pyramidal neurons. We also found a decrease in the density of CA2 parvalbumin-immunopositive interneurons and disruption to the pyramidal neuron-associated perisomatic perineuronal net in the CA2 subfield. These data reveal a set of pathological alterations that may disrupt inhibition of CA2 pyramidal neurons and their downstream targets in epileptic mice. 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/2022.11.09.515747v1?rss=1 Authors: Tang, M., Salvatori, T., Millidge, B., Song, Y., Lukasiewicz, T., Bogacz, R. Abstract: The computational principles adopted by the hippocampus in associative memory (AM) tasks have been one of the mostly studied topics in computational and theoretical neuroscience. Classical models of the hippocampal network assume that AM is performed via a form of covariance learning, where associations between memorized items are represented by entries in the learned covariance matrix encoded in the recurrent connections in the hippocampal subfield CA3. On the other hand, it has been recently proposed that AM in the hippocampus is achieved through predictive coding. Hierarchical predictive coding models following this theory perform AM, but fail to capture the recurrent hippocampal structure that encodes the covariance in the classical models. Such a dichotomy pose potential difficulties for developing a unitary theory of how memory is formed and recalled in the hippocampus. Earlier predictive coding models that learn the covariance information of inputs explicitly seem to be a solution to this dichotomy. Here, we show that although these models can perform AM, they do it in an implausible and numerically unstable way. Instead, we propose alternatives to these earlier covariance-learning predictive coding networks, which learn the covariance information implicitly and plausibly, and can use dendritic structures to encode prediction errors. We show analytically that our proposed models are perfectly equivalent to the earlier predictive coding model learning covariance explicitly, and encounter no numerical issues when performing AM tasks in practice. We further show that our models can be combined with hierarchical predictive coding networks to model the hippocampo-neocortical interactions. Our models provide a biologically plausible approach to modelling the hippocampal network, pointing to a potential computational mechanism employed by the hippocampus during memory formation and recall, which unifies predictive coding and covariance learning based on the recurrent network structure. 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/2022.11.09.515837v1?rss=1 Authors: Wang, L., Park, L., Wu, W., King, D., Medina, A. V., Raven, F., Martinez, J. D., Ensing, A., Yang, Z., Jiang, S., Aton, S. Abstract: Post-learning sleep plays an important role in hippocampal memory processing, including contextual fear memory (CFM) consolidation. Here, we used targeted recombination in activated populations (TRAP) to label context-encoding engram neurons in the hippocampal dentate gyrus (DG) and assessed reactivation of these neurons during post-learning sleep. We find that post-learning sleep deprivation (SD), which impairs CFM consolidation, selectively disrupts reactivation in inferior blade DG engram neurons. This change was linked to more general suppression of neuronal activity markers in the inferior, but not superior, DG blade by SD. To further characterize how learning and subsequent sleep or SD affect these (and other) hippocampal subregions, we used subregion-specific spatial profiling of transcripts and proteins. We found that transcriptomic responses to sleep loss differed greatly between hippocampal regions CA1, CA3, and DG inferior blade, superior blade, and hilus. Critically, learning-driven transcriptomic changes, measured 6 h following contextual fear learning, were limited to the two DG blades, differed dramatically between the blades, and were absent from all other regions. Similarly, protein abundance in these hippocampal subregions were differentially impacted by sleep vs. SD and by prior learning, with the majority of alterations to protein expression restricted to DG. Together, these data suggest that the DG plays an essential role in the consolidation of hippocampal memories, and that the effects of sleep and sleep loss on the hippocampus are highly subregion-specific, even within the DG itself. 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/2022.11.02.513937v1?rss=1 Authors: Keijzer, N., Oberman, K., Oroszi, T., Nyakas, C., van der Zee, E. A., Schoemaker, R. G. Abstract: Peripheral surgery may evoke neuroinflammation, associated with neuronal damage and consequently mental health problems. However, anti-inflammatory treatment showed limited therapeutic efficacy. Preservation of neuron integrity during neuroinflammation, by targeting their protective collagen sheet, may provide an alternative strategy. Whole-body vibration (WBV) and exercise combine anti-inflammatory and collagen-increasing effects in the periphery. The present study aimed to explore the therapeutic efficacy of postoperative WBV and exercise on hippocampal neuroinflammation and collagen expression. Three months old male Wistar rats underwent abdominal surgery. Starting from one day after surgery, rats were submitted to WBV (10 min, once or twice daily, 30 Hz), running exercise (30 min, daily), or pseudo WBV/exercise, for two weeks. Rats were sacrificed and brain tissue was collected and processed for (immuno)histochemistry. Hippocampal microglia activity, total collagen content, and expression of fibrous and non-fibrous collagen subtypes were analysed. Surgery was associated with increased microglia activity in the CA1 area, which was only partly reversed by the interventions. Surgery specifically reduced total collagen expression in the CA1 area, which was restored by both WBV and exercise. Collagen I was absent in the hippocampal granular layers. The surgery-induced decrease in collagen III expression in the CA1 area was not affected by either WBV or exercise. However, surgery increased collagen III in the CA2 (ns), CA3 and DG. Exercise, and to a lower extent WBV, seemed to (partly) reverse this effect. Collagen IV expression was not altered by surgery, but increased by WBV. No significant effects were observed on collagen VI expression. WBV as well as exercise restored the surgery-induced declined collagen expression, while partly reversing microglia activation in the CA1 area. Moreover, effects on collagen appeared to be subtype- and region-specific, with overall similar effects of WBV and exercise. Nevertheless, the neuroprotective potential of postoperatively altered brain collagen needs further investigation. 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/2022.11.01.514756v1?rss=1 Authors: Nagarajan, R., Lyu, J., Kambali, M., Wang, M., Courtney, C. D., Christian-Hinman, C. A., Rudolph, U. Abstract: Aging is often associated with a decline in cognitive function. A reduction in the number of somatostatin-positive (SOM+) interneurons in the DG has been described in cognitively impaired but not in unimpaired aged rodents. However, it remains unclear whether the reduction in SOM+ interneurons in the DG hilus is causal for age-related cognitive dysfunction. We hypothesized that hilar (SOM+) interneurons play an essential role in maintaining cognitive function and that a reduction in the number of hilar (SOM+) interneurons might be sufficient to induce cognitive dysfunction. Hilar (SOM+) interneurons were ablated by expressing a diptheria toxin transgene specifically in these interneurons. An AAV-EF1-mCherry-flex-dtA construct was stereotaxically injected (bilaterally) into the DG hilus of young adult Sst-IRES-Cre mice, which resulted in an approximately 50% reduction in the number of SOM+ neurons and also a reduction in the number of GAD-67+ neurons in the DG hilus. c-Fos staining was increased in DG and CA3 but not in CA1. Behavioral testing, which started 21 days after the stereotaxic injections, revealed a reduced recognition index in the novel object recognition test, a reduction in the percentage of correct alternations in the Y maze tests, and increased latencies and path lengths in the learning and the reversal learning phase of the Morris water maze. Our results show that partial genetic ablation of SOM+ hilar interneurons is sufficient to increase activity in DG and CA3, as has been described to occur with aging, and to induce an impairment of learning and memory functions. Thus, partial ablation of hilar SOM+ interneurons may be a significant contributing factor to age-related cognitive dysfunction. These mice may also be useful as a cellularly defined model of hippocampal aging. 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/2022.10.31.514574v1?rss=1 Authors: Zhuang, M., Geng, X., Han, P., Liang, F., Che, P., Liu, C., Yang, L., Yu, J., Zhang, Z., Dong, W., Ji, S.-J. Abstract: N6-methyladenosine (m6A) has been demonstrated to regulate learning and memory in mice. To investigate the mechanism by which m6A modification exerts its function through its reader proteins in the hippocampus, as well as to unveil the specific subregions of the hippocampus that are crucial for memory formation, we generated dentate gyrus (DG)-, CA3-, and CA1-specific Ythdf1 and Ythdf2 conditional knockout (cKO) mice, respectively. Surprisingly, we found that only the DG-specific Ythdf2 cKO mice displayed impaired memory formation, which is inconsistent with the previous report showing that YTHDF1 was involved in this process. YTHDF2 controls the stability of its target transcripts which encode proteins that regulate the elongation of mossy fibers (MF), the axons of granule cells in DG. DG-specific Ythdf2 ablation caused MF overgrowth and impairment of the MF-CA3 excitatory synapse development and transmission in the stratum lucidum. Thus, this study identifies the m6A reader YTHDF2 in dentate gyrus as the only regulator that mediates m6A modification in hippocampus-dependent learning and memory. 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/2022.10.27.514077v1?rss=1 Authors: Berndt, M., Trusel, M., Roberts, T. F., Volk, L. J., Pfeiffer, B. E. Abstract: Neuronal activity during experience is thought to induce plastic changes within the hippocampal network which underlie memory formation, although the extent and details of such changes in vivo remain unclear. Here, we employed a temporally precise marker of neuronal activity, CaMPARI2, to label active CA1 hippocampal neurons in vivo, followed by immediate acute slice preparation and electrophysiological quantification of synaptic properties. Recently active neurons in the superficial sublayer of stratum pyramidale displayed larger post-synaptic responses at excitatory synapses from area CA3, with no change in pre-synaptic release probability. In contrast, in vivo activity weakened both pre- and post-synaptic excitatory weights onto pyramidal cells in the deep sublayer. In vivo activity of deep and superficial neurons within sharp-wave ripples was bidirectionally changed across experience, consistent with the observed changes in synaptic weights. These findings reveal novel, fundamental mechanisms through which the hippocampal network is modified by experience to store information. 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/2022.10.24.513188v1?rss=1 Authors: Viana da Silva, S., Haberl, M. G., Gaur, K., Patel, R., Narayan, G., Ledakis, M., Fu, M. L., Koo, E. H., Leutgeb, J. K., Leutgeb, S. Abstract: Deficits in spatial navigation are among the early symptoms in Alzheimer's disease patients, consistent with the hippocampal formation as the site for spatial computations and disease onset. Although the correspondence between the early symptoms and brain regions that are affected early in the disease has been recognized, it is not clear whether progressive cognitive decline is solely caused by a spreading pathology or whether a focal pathology can by itself cause aberrant neuronal activity in a larger network. These possibilities cannot be distinguished in standard disease models which broadly express APP across brain regions. We therefore generated a mouse model in which the expression of mutant human APP was limited to hippocampal CA3 cells (CA3-APP mice). We first asked whether the limited pathology in CA3 can result in memory deficits and found impaired performance of CA3-APP mice in a hippocampus-dependent memory task. By then recording in the CA1 region, we asked to what extent neuronal activity patterns emerged in a brain region which received projections from APP-expressing CA3 cells, but did itself not show any primary pathology. While the spatial firing patterns of CA1 cells were preserved, we observed a reduced theta oscillation frequency in the local field potential and in a subpopulation of principal cells in CA1. Furthermore, CA1 interneurons showed decreased theta oscillation frequencies, and this effect was even more pronounced in CA3 interneurons, which also do not directly express APP. Pathology that is highly localized and limited to presynaptic cells is thus sufficient to cause aberrant firing patterns in postsynaptic neuronal networks, which indicates that disease progression is not only from a spreading molecular pathology but also mediated by progressive physiological dysfunction. 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/2022.10.23.513396v1?rss=1 Authors: Kruse, P., Vlachos, A., Lenz, M. Abstract: Neurological diseases can lead to the denervation of brain regions caused by demyelination, traumatic injury or cell death. Nevertheless, the molecular and structural mechanisms underlying the lesion-induced reorganization of denervated brain regions are a matter of ongoing investigation. In order to address this issue, we performed an entorhinal cortex lesion (ECL) in organotypic entorhinal-hippocampal tissue cultures and studied denervation-induced homeostatic plasticity of mossy fiber synapses, which connect dentate granule cells with CA3 pyramidal neurons and play important roles in spatial learning. Partial denervation caused a homeostatic strengthening of excitatory neurotransmission in dentate granule cells (GC), in CA3 pyramidal neurons, and their direct synaptic connections as revealed by paired recordings (GC-to-CA3). These functional changes were accompanied by ultrastructural reorganization of mossy fiber synapses, which regularly contain the plasticity-related protein synaptopodin and the spine apparatus organelle. We demonstrate that the spine apparatus organelle and its associated protein synaptopodin assemble ribosomes in close proximity to synaptic sites and moreover we unravel synaptopodin-related transcriptome, which can be linked to the expression of homeostatic synaptic plasticity. Notably, synaptopodin-deficient tissue preparations that lack the spine apparatus organelle, failed to express homeostatic adjustments of both excitatory neurotransmission and the region-specific transcriptome. Hence, synaptopodin and the spine apparatus organelle form local protein synthesis hubs that are essential for mediating lesion-induced homeostatic synaptic plasticity. 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/2022.10.17.512498v1?rss=1 Authors: Douchamps, V., di Volo, M., Torcini, A., Battaglia, D., Goutagny, R. Abstract: The hippocampus and the entorhinal cortex display a rich oscillatory activity, believed to support neural information processing in key cognitive functions. In the hippocampal region CA1, a slow gamma rhythm (30-80 Hz) generated in CA3 would support memory retrieval whereas a medium gamma rhythm (60-120 Hz) generated in the entorhinal cortex would support memory encoding. However, descriptions involving discrete gamma sub-bands can only partially account for the haphazard diversity of oscillatory behaviors observed in individual recordings during spatial navigation behavior. Here, we stress that transient gamma oscillatory episodes at any frequency or phase relative to the ongoing theta (4-12 Hz) rhythm can be recorded at any layer within CA1. Eventually, the commonly reported averages are dominated by a minority of very strong power events overshadowing gamma heterogeneity. Nevertheless, we show that such gamma diversity can be naturally explained by a simple mechanistic model, and that behavior-related information (position within a maze) can be decoded from most individual gamma events, despite their low power and erratic-like nature. Our results indicate that behavior specifically shapes ensembles of irregular hippocampal gamma oscillations, in a way which evolves with learning, depends on the hippocampal layer and is hard to reconcile with the hypothesis of rigid, narrowly tuned gamma sub-bands. Beyond randomness, the pervasive gamma diversity may thus reflect complexity at the "fringe-of-synchrony" likely functional but invisible to classic average-based analyses. 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/2022.10.05.511002v1?rss=1 Authors: Lyu, J., Nagarajan, R., Kambali, M., Wang, M., Rudolph, U. Abstract: The cellular basis of age-related impairments of hippocampal function is not fully understood. In order to evaluate the role of somatostatin-positive (Sst+) interneurons in the dentate gyrus hilus in this process, we chemogenetically inhibited Sst+ interneurons in the dentate gyrus (DG) hilus. Chronic chemogenetic inhibition (CCI) of these neurons resulted in increased c-Fos staining in the DG hilus, a decrease in the percentage of Gad67- and of Sst-expressing neurons in the DG, and increased microglial activation in DG, CA3, and CA1. Total dendritic length and spine density were reduced in DG and CA1, suggesting reduced dendritic complexity. Behaviorally, the recognition index in an object recognition task and the percentage of spontaneous alternations in the Y maze were decreased, while in both initial and reversal learning in the Morris water maze the latencies to find the hidden platform were increased, suggesting cognitive dysfunction. Our findings establish a causal role for a reduced function of Sst+ interneurons in the DG hilus for cognitive decline and suggest that this reduced function may contribute to age-related impairments of learning and memory. Our CCI mice may represent a cellularly defined model of hippocampal aging. 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/2022.09.27.509638v1?rss=1 Authors: Rosenberg, E., Chamberland, S., Bazelot, M., Nebet, E., Wang, X., McKenzie, S., Jain, S., Greenhill, S., Wilson, M., Salah, A., Bailey, S., Patra, P. H., Chenouard, N., Sun, S., Jones, D., Buzsaki, G., Devinsky, O., Woodhall, G., Scharfman, H., Whalley, B., Tsien, R. Abstract: Cannabidiol (CBD), a non-euphoric component of cannabis, reduces seizures in multiple forms of pediatric epilepsy, but the mechanism(s) of anti-seizure action remain unclear. In one leading model, CBD acts at glutamatergic axon terminals, blocking pro-excitatory actions of an endogenous membrane phospholipid, lysophosphatidylinositol (LPI), at the G protein-coupled receptor GPR55. However, the impact of LPI-GPR55 signaling at inhibitory synapses and in epileptogenesis remains underexplored. We found that LPI transiently increased hippocampal CA3 to CA1 excitatory presynaptic release probability and evoked synaptic strength in WT mice, while attenuating inhibitory postsynaptic strength by decreasing GABAAR gamma 2 and gephyrin puncta. Effects of LPI at both excitatory and inhibitory synapses were eliminated by CBD pretreatment and absent after GPR55 deletion. Acute pentylenetrazole-induced seizures elevated levels of GPR55 and LPI, and chronic lithium pilocarpine-induced epileptogenesis potentiated the pro-excitatory effects of LPI. We propose that CBD exerts potential therapeutic effect both by blocking synaptic effects of LPI and dampening hyperexcitability. 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/2022.09.14.507576v1?rss=1 Authors: Mugnaini, M., Trinchero, M. F., Schinder, A. F., Piatti, V. C., Kropff, E. Abstract: Mammalian hippocampal circuits undergo extensive remodeling through adult neurogenesis. While this process has been widely studied, the specific contribution of adult-born granule cells (aGCs) to spatial operations in the hippocampus remains unknown. Here we show that optogenetic activation of 4-week-old (young) aGCs in free-foraging mice produces a non-reversible reconfiguration of spatial maps in proximal CA3, while rarely evoking neural activity. Stimulation of the same neuronal cohort on subsequent days recruits CA3 neurons with increased efficacy but fails to induce further remapping. In contrast, stimulation of 8-week-old (mature) aGCs can reliably activate CA3 cells but produce no alterations in spatial maps. Our results reveal a unique role of young aGCs in remodeling CA3 representations, a potential that can be depleated and is lost with maturation. This ability could contribute to generate orthogonalized downstream codes supporting pattern separation. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

AlabamaSeveral states have primary elections today, Alabama will do the same next weekCongressman Aderholt seeks timeline on  Space Command coming to HuntsvilleA shooting  in Buffalo, NY has ties to Tuscaloosa woman, she loses younger sisterGas prices in Alabama and other states goes up 15 cents per gallon in one weekA statue honoring Heavyweight Champion Deontay Wilder to be unveiled this weekNationalSCOTUS rules 6 to 3 on a campaign fund law involving TX senator Ted CruzMore details emerge on church shooting in Laguna Woods, CA3 way dead heat in PA with GOP Senate primary candidatesDonald Trump promotes NC congressman Madison Cawthorn for re-electionMars-Wrigley candy maker issues recall of 3 types of gummies due to metal strands

In this episode I'm featuring a chat I had on another podcast. CA3's Cup of Tea series is hosted by Sarah Wardle. Sarah's also an ex-teammate from back in the day when she was starting out in the industry. So it was great catching up with her. Onboarding is a big part of their business [they've some great onboarding tech call Eli]. So this episode is about content marketing and what it means for onboarding. Enjoy the chat and don't forget to subscribe or follow to both podcasts. Links that we mentioned: The Cup of Tea series podcast: https://anchor.fm/ca3 CA3's onboarding software, Eli: https://www.cathree.com/onboarding/ The Daily Goat Vlog: https://www.linkedin.com/company/the-goat-agency/videos/ The WeAreNetflix podcast: https://www.chrislch.com/post/podcasts-the-next-big-format-in-employer-marketing RAD Award winner: https://radawards.com/2020/en/page/2020-winners --- Send in a voice message: https://anchor.fm/employercontentmarketing/message

2:25 Left Coast CrossFit in Laguna Niguel, CA3:58 Battle Cancer Aims to Kick Cancer to the Dust4:30 Step One: Be Mindful of Your Environment4:45 Airbnb 6:39 Counting Macros7:11 EPIC Bars or RXBAR7:55 Sean Sweeney8:17 C4 Cellucor Pre-Workout9:20 Step Two: Increase Your Steps 11:45 Grounding13:26 Acclimate to the time and get morning sun15:18 Step Three: Be Mindful of Your Nutrition17:00 Chelsea Bun 19:29 Intermittent Fasting22:35 Step Four: Plan to Train As You Can 24:03 CrossFit Shapesmiths and Outside the Box Holidays24:19 VoyEdgeRX30:12 Be a good drop-inFollow Morning Chalk Up: https://www.instagram.com/morningchalkup/. Follow Jessica Danger: https://www.instagram.com/mamadanger/. Follow Brittany Marsh: https://www.instagram.com/the_brittumentary/. Email us at: Jessica@morningchalkup.com.

Just to clarify this somewhat oddly-flowing podcast episode, it was originally broadcast live on Indy In-Tune Radio one Saturday afternoon as a "Jeff DeHerdt Listening Party" where we played his new release, Ghost Museum, in its entirety over the course of an entire afternoon. Sadly, about fifteen minutes in, my trusty 15-year-old laptop decided to reboot itself (it has never done this before, or since), causing us to lose the actual introduction to Jeff and his album, and making it really difficult to piece a new one out of the various conversations we had over the rest of the afternoon. (Jeff and I are notorious for just geeking out on off-topic conversations, usually involving comic books, scifi or obscure old bands.) Therefore, it's going to feel like you got dropped in the middle of a conversation, which technically you did. In fact, you're also hearing what was literally a four and a half-hour rambling conversation that I've somehow paired down to one hour. It was worth it though. Jeff DeHerdt is a long-time friend of the show, one of my favorite musicians to go see, and obviously one of my favorite people to sit and talk to for hours on end about every topic under the sun. With Ghost Museum, he continues his musical evolution that started almost 15 years ago with the largely jazz-related Club Bordeau, through the popjazz AOR of Autumn House, and into still another very different realm, this time drawing on sounds and stylings of late new wave influenced pop, but adding a more refined modern sophistication to it that makes it less of a tribute or mashup and more of a love letter. Links Referenced in the Show: Jeff DeHerdt can be found here: | | Information about his latest project, Ghost Museum, can be found . All three of his CD's (that he owns up to #TheBlueAlbumExists) can be found at the usual suspects: | | | . His first appearance on Indy In-Tune was with his experimental electronic band CA3 back on . He has since appeared on and , plus a couple of guest-host appearances if you skim through the library. He's playing three Friday nights in December with drummer, Michael Beck, from and .