Podcasts about hippocampal

This week on the show, we're have our sights set on healthy aging. What would it mean to be able to live to 80, 90 or 100 with our cognitive abilities intact and able to maintain an independent lifestyle right to the end of our days? We're joined by Beth Mormino and Anthony Wagner who lead the Stanford Aging and Memory Study, which recruits cognitively healthy older adults to understand what makes their brains particularly resilient — and how more of us could join them in living the dream of healthy aging.Learn MoreStanford Aging and Memory Study (SAMS)Stanford Memory LabMormino LabFurther ReadingAlzheimer's 'resilience signature' predicts who will develop dementia—and how fast (Knight Initiative for Brain Resilience, 2025)Latest Alzheimer's lab tests focus on memory loss, not brain plaques (NPR, 2025)ReferencesTrelle, A. N., ... & Wagner, A. D. (2020). Hippocampal and cortical mechanisms at retrieval explain variability in episodic remembering in older adults. eLife, 9:e55335. doi: 10.7554/eLife.55335 PDF | PMID:32469308Trelle, A. N., ..., Wagner, A. D., Mormino, E. C., & Wilson, E. N. (2025). Plasma Aβ42/Aβ40 is sensitive to early cerebral amyloid accumulation and predicts risk of cognitive decline across the Alzheimer's disease spectrum. Alzheimer's & Dementia, 21:e14442. PDF | PMID:39713875Sheng, J., ..., Mormino, E., & Wagner, A. D. (submitted). Top-down attention and Alzheimer's pathology impact cortical selectivity during learning, influencing episodic memory in older adults.  PreprintEpisode CreditsThis episode was produced by Michael Osborne at 14th Street Studios, with sound design by Morgan Honaker. Our logo is by Aimee Garza. The show is hosted by Nicholas Weiler at Stanford's Wu Tsai Neurosciences Institute and supported in part by the Knight Iniative for Brain Resilience.Get in touchWe want to hear from your neurons! Email us at at neuronspodcast@stanford.edu if you'd be willing to help out with some listener rSend us a text!Thanks for listening! If you're enjoying our show, please take a moment to give us a review on your podcast app of choice and share this episode with your friends. That's how we grow as a show and bring the stories of the frontiers of neuroscience to a wider audience. Learn more about the Wu Tsai Neurosciences Institute at Stanford and follow us on Twitter, Facebook, and LinkedIn.

We spend so much time focusing on how exercise changes our bodies - burning calories, building muscle, shedding fat. What if the most important transformation is happening where you can't see it? Hidden inside your skull, your brain is changing with every step, squat, and sprint. Neuroscientist Dr. Wendy Suzuki has spent years uncovering how movement rewires the brain. As a professor at NYU and an expert in neuroplasticity, Wendy's research reveals how aerobic exercise boosts memory, sharpens focus, and even builds a protective barrier against dementia. In this episode, Wendy explains what happens inside your brain when you move, why it's never too late to strengthen your mind, and the powerful ways exercise can slow brain aging. You'll discover simple, science-backed habits - including her own brain-boosting routine - to help you stay mentally sharp for years to come.

Although Alzheimer disease (AD) is the most common neurodegenerative cause of dementia, other etiologies can mimic the typical amnestic-predominant syndrome and medial temporal brain involvement. Neurologists should recognize potential mimics of AD for clinical decision-making and patient counseling. In this episode, Kait Nevel, MD, speaks with Vijay K. Ramanan, MD, PhD, an author of the article “LATE, Hippocampal Sclerosis, and Primary Age-related Tauopathy,” in the Continuum December 2024 Dementia issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Ramanan is a consultant and assistant professor of neurology in the Division of Behavioral Neurology at Mayo Clinic College of Medicine and Science in Rochester, Minnesota. Additional Resources Read the article: LATE, Hippocampal Sclerosis, and Primary Age-related Tauopathy Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: IUneurodocmom Guest: @vijaykramanan Full episode transcript available here Dr Jones: This is Dr Lyle Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum 's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum Journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Nevel: This is Dr Kait Nevel. Today I'm interviewing Dr Vijay Ramanan about his article he wrote with Dr Jonathan Graff-Radford on LATE hippocampal sclerosis and primary age-related tauopathy, which appears in the December 2024 Continuum issue on dementia. Welcome to the podcast. Vijay, can you please introduce yourself to the audience? Dr Ramanan: Thanks so much, Kait. I'm delighted to be here. So, I am a cognitive neurologist and neuroscientist at the Mayo Clinic in Rochester, Minnesota. I have roles in practice, education and research, but amongst those I see patients with cognitive disorders in the clinic. I help direct our Alzheimer's disease treatment clinic and also do research, including clinical trial involvement and some observational research on genetics and biomarkers related to Alzheimer's and similar disorders. Dr Nevel: Great, thanks for that. So, I'd like to start off by talking about why is LATE hippocampal sclerosis, why is this important for the neurologist practicing in clinic to know about these things? Dr Ramanan: That's a great question. So, if we take a step back, we know that degenerative diseases of the brain are really, really common, and they get more and more common as we get older. I think all neurologists, and in fact most clinicians and large swaths of the general public, are well aware of Alzheimer's disease, which is the most common degenerative cause of cognitive impairment in the population. But there are non-Alzheimer's degenerative diseases which can produce cognitive difficulties as well. And it's important to be aware of those disorders, of their specific presentations and their implications, in part because it's always a healthy thing when we can be as precise and confident about diagnosis and expectation with our patients as possible. I'll look to the analogy of a patient presenting with a myelopathy. As neurologists, we would all find it critical to clarify, is that myelopathy the result of a compressive spondylotic change? The result of an inflammatory disorder, of a neoplastic disorder, of an infectious disorder? It's critical to guide the patient and choose appropriate management options based on the cause of their syndrome. It would potentially harm the patient if you treated an infectious myelopathy with steroids or other immune-suppressant drugs. So, a similar principle holds in cognitive neurology. I accept with humility that we can never be 100% crystal clear certain about things in medicine, just because when you think you got it all figured out there's a curveball. But I want to get as close to that 100% as possible. And recognizing that disorders like LATE or PART can mimic the symptoms, sometimes even the imaging features of Alzheimer's disease. I think it's critical to have heightened awareness of those disorders, how they look, to be able to apply appropriate counseling and management options to patients. I think this becomes particularly critical as we move into an era of disease-specific, and sometimes disease-modifying, therapies, where applying a choice of a treatment option could have significant consequences to a patient if the thing you're treating isn't the thing that the drug is trying to accomplish. So, having awareness and spreading awareness about some of these non-AD causes of cognitive difficulty, I think, is a big mission in the field.  Dr Nevel: Yeah, that makes total sense. And kind of leaning into this, you know, trying to differentiate between these different causes of late-life amnestic cognitive impairment. You know, I'll point out to the listeners today to please read your article, but in addition to reading your article, I'd like to note that there's a really nice table in your article, Table 6-1, where you kind of go through the different causes of amnestic cognitive impairment and the different features that better fit with diagnosis X, Y, or Z, because I think it's a really nice table to reference and really easy to look at and reference back to. But on that note, what is your typical approach when you're seeing a patient in clinic, have a new referral for an older patient presenting with a predominantly progressive amnestic-type features? Dr Ramanan: Excellent question. And this is one that I think has relevance not just in a subspecialty memory clinic, but to all the clinicians who help to diagnose and manage cognitive disorders, including in primary care and general neurology and others. One principle that I think it's helpful to keep in our minds is that in cognitive neurology, no one data point takes precedence over all the others. We have a variety of information that we can gather from history, from exam, from imaging, from fluid biomarkers. And really the fun, the challenge, the reward is in piercing together that information. It's almost like being a lawyer and compiling the evidence, having possibilities on your list and raising and lowering those possibilities to get as close to the truth as you can. So, for patients with a cognitive syndrome, I think the first plank is in defining that syndrome. As you mentioned, if I'm seeing someone with a progressive amnestic-predominant syndrome, I first want to make sure, are we talking about the same thing, the patient, the care partner, and I?  Can often be helpful to ask them for some examples of what they see, because sometimes what patients may report as memory troubles may in fact reflect cognitive difficult in other parts of our mental functioning. For example, executive functioning or naming of objects. And so helpful to clarify that in the history to get a sense of the intensity and the pace of change over time, and then to pair that with a good general neurologic exam and some type of standardized assessment of their cognitive functioning. At the Mayo Clinic, where partial to the short test of mental status. There are other ways to accomplish that, such as with an MMSE or a MoCA. If I understand that the syndrome is a progressive amnestic disorder, Alzheimer's disease is the most common cause of that presentation in older adults, it deserves to be on my differential diagnosis. But there might be some other features in the story that could raise or lower those mimics on my list. So, in patients who are, say, older than the age of seventy five, disorders like LATE or PART start to rise higher on the likelihood for me, in particular if I know that their clinical course has been more slow brewing, gradually evolving. And again, most degenerative disorders we expect to evolve not over days or weeks, but over many months to many years. But in comparison with Alzheimer's disease, patients with LATE or with PART would be expected to have a little more slow change where maybe year over year they or their care partners really aren't noticing big declines. Their daily function is relatively spare. There might not be as much involvement into other non-memory cognitive domains. So, these are some of the pieces of the story that can help to perhaps isolate those other non-AD disorders on the list as being more likely and then integrating, as a next level, diagnostic testing, which helps you to rule in and rule out or support those different causes. So, for example, with LATE there can be often out of proportion to the clinical picture, out of proportion to what you see on the rest of their imaging or other profiles, very predominant hippocampal and medial temporal volume loss. And so that can be a clue in the right setting that you may not be dealing with Alzheimer's disease or pure Alzheimer's disease, but that this other entity is there. So, in the big picture, I would say being systematic, recognizing that multiple data points being put together helps you get to that confident cause or etiology of the syndrome. And in particular, taking a step back and thinking about big picture factors like age and course to help you order those elements of the differential, whether AD or otherwise. Dr Nevel: Great, thanks. In your article, you talk about different imaging modalities that can be used, as you mentioned, you know, just another piece of the puzzle, if you will, to try and put together what may be going on with the patient, and recognizing that some of these imaging techniques are imaging is special imaging, not available in a lot of places.  You know, and maybe other diagnostic type tests that could be helpful in differentiating between these different disorders may not be available, you know, for the general neurologist practicing in the community. So, what do you suggest to the general neurologist maybe practicing somewhere where they don't have access to some of these ancillary tests that could assist with a diagnosis?  Dr Ramanan: Critical question. And here I think there's not likely to be one single answer. As with most things, awareness and recognition is a good place to start. So, some of those clues that I mentioned earlier about the clinical course, about the age, the- we're talking about clinical setting there. So, comfort with and understanding that the clinical setting can help you to be more confident about, for example, LATE or PART being present in contrast to AD. That's important information. It deserves to be part of the discussion. It doesn't necessarily need other tests to have value on its own. A second piece is that tests help, in some cases, to rule in and rule out causes for cognitive difficulty. As part of a standard cognitive evaluation, we would all be interested in getting some blood tests to look for thyroid dysfunction or vitamin deficiencies. Some type of structural head imaging to rule out big strokes, tumors, bleeds. Head CT can accomplish some of that perspective. It's ideal if a brain MRI can be obtained, but again, keeping in mind, what's the primary goal of that assessment? It's to assess structure. Occasionally you can get even deeper clues into a syndrome from the MRI. For example, that very profound hippocampal or medial temporal atrophy. So, increasing awareness amongst clinicians throughout our communities to be able to recognize that change and put it in the context of what they see in other brain regions that can be affected by Alzheimer's or related disorders. For example, the parietal regions can be helpful. And recall that MRI can also be helpful in assessing for chronic cerebrovascular disease changes. This is another mimic that shows up in that table that you mentioned. And so multiple purposes can be satisfied by single tests. Now, you're absolutely right that there are additional test modalities that, perhaps in a subspecialty clinic at an academic medical center, we're very used to relying on and finding great value on; for example, glucose PET scans or sometimes fluid biomarkers from the blood or from the spinal fluid. And these are not always as widely available throughout our communities. Part of the challenge for all of us as a field is therefore to take the expertise that we have gathered in more subspecialty settings and tertiary care settings and translate and disseminate that out into our communities where we need to take care of patients. That's part of the challenge. The other challenge is in continued tool and technological development. There's a lot of optimism in our field that the availability of blood-based biomarkers relevant for Alzheimer's disease may play a part in helping to address some of the disparities in resource and access to care. You can imagine that doing a blood test to give you some high-quality information, there are going to be less barriers to doing that in many settings compared to thinking about a lumbar puncture or a PET scan, both in terms of cost to the patient as well as infrastructure to the clinicians and the care team. So I'm optimistic about a lot of those changes. In the meantime, I think there are, through both clinical evaluation and some basic testing including structural head imaging, there are clues that can help navigate these possibilities. Dr Nevel: So, let's say you have your patient in clinic, you've done your evaluation, maybe gotten some ancillary testing, and you highly suspect either LATE or PART. How do you counsel those patients and their families? How do you manage those patients moving forward who you really suspect don't have, you know, some sort of co-pathology? Dr Ramanan: So, it's- I think it's helpful to remember when patients are coming to see us, either they or the people around them have noticed an issue. And very likely it's an issue that's been brewing for a little while. I think it can be very valuable, very helpful for patients to have answers. What's the cause for the issue? Once you have answers, even if sometimes those answers are not the most welcome things or the things that you'd be looking forward to, answers give you an opportunity to grab hold of what's going on, to define a game plan. So, understanding there is a degenerative disease there, it sheds light on why that individual had had memory symptoms over the years. And it gives them a general expectation that over time on an individualized basis, but generally expecting gradually over many months to many years, there may be some worsening in some of those symptoms helps them to plan and helps them to make the adaptations that are a-ok and great to make to just help you to do the things you want to do. As much as I can, I try to put the focus here closer to how we would view things like high blood pressure or high cholesterol. Those are also chronic issues that tend to be more common as we get older, tend to get more troublesome as we get older. The goal is, know what you're dealing with and take the combination of lifestyle modifications, adaptations in your day-to-day and maybe medications to keep them as mild and as slow-changing as possible. With something like LATE, we don't have specific medication therapies to help support cognitive functioning at this time. There's a lot of hope that with additional research we will have those therapies. But even so, I think it's an important moment to emphasize some of those good healthy lifestyle habits. Staying mentally, socially and physically active, getting a good night's sleep, eating a healthy, balanced diet, keeping good control of vascular risk factors, all of that is critical to keeping the brain healthy, keeping the degenerative disease as mild and slow-brewing as possible. And understanding what some of the symptoms to expect could be. So, with LATE the syndrome tends to be very memory-predominant. There may be some trouble with maybe naming of objects or perhaps recall of emotionally salient historical knowledge, world events, but you're not expecting, at least over the short to medium term, huge intervening on other cognitive functioning. And so that can be helpful for patients to understand. So, the hope is once you know what what you're dealing with, you understand that the disease can look different from person to person. Having a general map of what to expect and what you can do to keep it in check, I think, is the goal. Dr Nevel: I agree with you 100% that it really can be helpful even if we can't, quote unquote, fix it, that for people, family, the patient have a name for what they have and kind of have some sort of idea of what to expect in the future. And they may come in thinking that they have Alzheimer's or something like that. And then, so, to get that information that this is going to be a little different, we expect this to go a little bit differently then it would if you had a diagnosis of Alzheimer's, I can see how that would be really helpful for people.  Dr Ramanan: I completely agree. And here's another challenge for us in the field when most patients have heard about Alzheimer's disease and many have perhaps even heard of dementia with Lewy bodies or frontotemporal dementia, but may not have heard of things like LATE. And they're not always easy to go online or find books that talk about these things. Having a name for it and being able to pair that with patient-friendly information is really critical. I see our appointments where we're sharing those diagnosis and making initial game plans as an initial foray into that process.  Dr Nevel: Yeah, absolutely. What is the greatest inequity or disparity that you see in taking care of patients with progressive amnestic cognitive impairment? Dr Ramanan: Yeah, great question. I think two big things come to mind. The first, you hinted at very well earlier that there are disparities in access to care, access to diagnostic testing, access to specialists and expertise throughout our communities. If we want diagnostics and therapeutics to be broadly applicable, they do need to be broadly available. And that's a big challenge for us as a field to work to address those disparities. There's not going to be one single cause or contributor to those iniquities, but as a field, I'm heartened to see thought and investment into trying to better address those. Another big weakness, and this is not just limited to cognitive neurology, it's a challenge throughout neurology, is that too many of our research studies are lacking in diversity. And that impacts our biological and pathophysiological understanding of these disorders. It also impacts our counseling and management. Again, if we want a new drug treatment to be broadly applicable throughout all of the patients that we take care of, we need to have data which guides how we apply those treatments. And so again, I'm heartened. This is a big challenge. It's a long standing challenge. It will take deep and long standing committed efforts to reverse. But I'm heartened that there are efforts in the field to broaden clinical trial enrollment, broaden observational research enrollment, and again, broaden access to tools and expertise. As a neurologist, I got into this field because I want to help people, use my expertise and my training to help people. These are steps that we can take to make sure that that help is broadly applicable throughout everybody in our communities. Dr Nevel: Yeah, absolutely. So, kind of segueing from you mentioning research and how we can better include patients in research. What do you think the next breakthrough is going to be? What do you think the next big thing is going to be in these disorders? What do we still need to learn? Dr Ramanan: There's a lot. I think for LATE and PART, the development of specific biomarkers would be top of the agenda. Now, biomarkers are by their nature imperfect. Even with Alzheimer's disease, where in comparison, we know quite a lot. We have a variety of imaging and fluid biomarkers that we can use to support or rule out a diagnosis. There are nuances in how you interpret those biomarkers. Patients can have signs of amyloid plaques in their brain and have completely normal cognition. They may be at risk for developing cognitive trouble due to Alzheimer's disease in the future, but it's one piece of the puzzle. Patients can have the changes of Alzheimer's disease amyloid plaques and tau tangles in the brain. We can confirm that through biomarkers. But at the end of the day, their cognitive syndrome might be driven by something else. Maybe it's Lewy body disease, maybe it's LATE, maybe it's a combination of factors. So, integrating and interpreting those biomarkers is challenging. But I do think, again, from the standpoint of giving patients answers with a diagnosis, having those biomarkers is really critical to just kind of closing the loop. It will also be critical to have those biomarkers as we're assessing for treatment response. So, for example, patients who may have coexistent Alzheimer's disease and LATE, I don't think we know the answer fully as to how likely they are to benefit from, say, newer antiamyloid monoclonal antibodies for Alzheimer's disease in the setting of that second pathology. So, wouldn't it be great if, similar to an oncologic setting where you engage in a treatment and then you're tracking two or three or four plasma measures and you're tracking tumor size with imaging, if we had this multimodal ability to track neurodegenerative pathology through biomarkers? I think that'll be a critical next step. And so, filling out that for non-Alzheimer's diseases, including LATE and PART, I think is item number one on the agenda. Dr Nevel: Wonderful, thank you so much. I really appreciate you taking the time to chat with me today about your article. I really enjoyed our conversation, certainly learned a lot. Dr Ramanan: Thank you so much, Kait. Love talking with you. And again, it was an honor to write this article. I hope it's helpful to many out in the field who take care of patients with cognitive issues.  Dr Nevel: Yeah, I think it will be. So again, today I'm interviewing Dr Vijay Ramanan about his article that he wrote with Dr Jonathan Graff-Radford on LATE hippocampal sclerosis and primary age-related tauopathy, which appears in the most recent issue of Continuum on dementia. Be sure to check out Continuum audio episodes from this and other issues. And thank you, Vijay, and thank you to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use this link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/AudioCME. Thank you for listening to Continuum Audio.

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Previously thought to be mere connective tissue and support for neurons, astrocytes are now understood to have many functions in the nervous system that are linked with seizures and epilepsy. Dr. Cecilie Nome spoke with Dr. Peter Bedner about astrocytes' involvement in epilepsy and how identifying and resolving astrocyte dysfunction is a new frontier in drug development.Relevant articles:de Ceglia R., et al. 2023. Specialized astrocytes mediate glutamatergic gliotransmission in the CNS. Nature 622, 120–129.Grote A., et al. 2023. ‘Hippocampal innate inflammatory gliosis only' in pharmacoresistant temporal lobe epilepsy. Brain 146(2), 549-560.Ravi V.M., et al. 2015. Astrocyte uncoupling as a cause of human temporal lobe epilepsy. 2015. Brain 138(5), 1208-1222. Support the Show.Sharp Waves episodes are meant for informational purposes only, and not as clinical or medical advice.Let us know how we're doing: podcast@ilae.org.The International League Against Epilepsy is the world's preeminent association of health professionals and scientists, working toward a world where no person's life is limited by epilepsy. Visit us on Facebook, X (Twitter), Instagram, and LinkedIn.

Mary Kate Joyce discusses her paper, “Subgenual and Hippocampal Pathways in Amygdala Are Set to Balance Affect and Context Processing,” published in Vol. 43, Issue 17 of JNeurosci in 2023, with Megan Sansevere from SfN's Journals' staff. Find the rest of the Spotlight collection here. With special guest: Mary Kate Joyce Hosted by: Megan Sansevere On Neuro Current, we delve into the stories and conversations surrounding research published in the journals of the Society for Neuroscience. Through its publications, JNeurosci, eNeuro, and the History of Neuroscience in Autobiography, SfN promotes discussion, debate, and reflection on the nature of scientific discovery, to advance the understanding of the brain and the nervous system.  Find out more about SfN and connect with us on X, Instagram, and LinkedIn.  

Welcome to the 18th episode of The Brain Podcast - the official podcast of the journals Brain and Brain Communications.  This episode features a discussion with first author author Dr Stefanie Grabrucker of the Brain article entitled: Microbiota from Alzheimer's patients induce deficits in cognition and hippocampal neurogenesis How does lifestyle and the environment affect cognition in Alzheimer's disease via the gut and what can we do about it? Listen for this and more in this exciting episode. Check out the full article on the Brain website: https://doi.org/10.1093/brain/awad303 This episode was co-hosted by Chaitra Sathyaprakash and Adam Handel,  edited and produced by Chaitra and Xin You Tai, co-produced by Antonia Johnston, original music by Ammar Al-Chalabi.

Powerful large-scale AI models like GPT-4 are showing dramatic improvements in reasoning, problem-solving, and language capabilities. This marks a phase change for artificial intelligence—and a signal of accelerating progress to come.In this Microsoft Research Podcast series, AI scientist and engineer Ashley Llorens hosts conversations with his collaborators and colleagues about what these models—and the models that will come next—mean for our approach to creating, understanding, and deploying AI, its applications in areas such as health care and education, and its potential to benefit humanity.This episode features Principal Researcher Ida Momennejad. Momennejad is applying her expertise in cognitive neuroscience and computer science to better understand—and extend—AI capabilities, particularly when it comes to multistep reasoning and short- and long-term planning. Llorens and Momennejad discuss the notion of general intelligence in both humans and machines; how Momennejad and colleagues leveraged prior research into the cognition of people and rats to create prompts for evaluating large language models; and the case for the development of a “prefrontal cortex” for AI.Learn more:AI and Microsoft Research | Focus AreaEvaluating Cognitive Maps and Planning in Large Language Models with CogEval | Publication, October 2023Imitating Human Behaviour with Diffusion Models | Publication, May 2023Navigates Like Me: Understanding How People Evaluate Human-Like AI in Video Games | Publication, April 2023Navigation Turing Test (NTT): Learning to Evaluate Human-Like Navigation | Publication, July 2021Predictive Representations in Hippocampal and Prefrontal Hierarchies | Publication, January 2022The successor representation in human reinforcement learning | Publication, September 2017Encoding of Prospective Tasks in the Human Prefrontal Cortex under Varying Task Loads | Publication, October 2013

Nachum Ulanovsky is a professor at the Weizman Institute. We talk about his research on spatial navigation in bats, how Nachum started working with bats, the importance of natural behaviour, how to build a 700m long tunnel for neuroscience, and much more.Support the show: https://geni.us/bjks-patreonTimestamps0:00:00: How Nachum started working with bats0:09:29: The technical difficulties of working with bats and in a new species0:16:03: The Egyptian Fruit Bat0:19:42: Wild bats vs lab-born bats / spatial navigation in very large spaces0:26:28: How to build a 700m long tunnel for neuroscience0:44:30: 2 random questions about bats0:53:48: The social lives of bats & social place cells1:05:09: Why are there so many types of cells for spatial navigation?1:13:01: Natural neuroscience1:17:33: A book or paper more people should read1:20:39: Advice for PhD students/postdocsPodcast linksWebsite: https://geni.us/bjks-podTwitter: https://geni.us/bjks-pod-twtNachum's linksWebsite: https://geni.us/ulanovsky-webBen's linksWebsite: https://geni.us/bjks-webGoogle Scholar: https://geni.us/bjks-scholarTwitter: https://geni.us/bjks-twtReferences & linksBracken Cave in Texas, with millions of bats: https://www.youtube.com/watch?v=PNPioS_roREThe Onion video on scientist who wasted life studying anteaters: https://www.youtube.com/watch?v=qXD9HnrNrvkEilam-Altstadter ... (2021). Stereotaxic brain atlas of the Egyptian fruit bat.Eliav ... (2021). Multiscale representation of very large environments in the hippocampus of flying bats. Science.Finkelstein ... (2015). Three-dimensional head-direction coding in the bat brain. Nature.Geva-Sagiv ... (2015). Spatial cognition in bats and rats: from sensory acquisition to multiscale maps and navigation. Nat Rev Neuro.Geva-Sagiv ... (2016). Hippocampal global remapping for different sensory modalities in flying bats. Nat Neuro.Hafting ... (2005). Microstructure of a spatial map in the entorhinal cortex. Nature.Hodgkin & Huxley (1952). A quantitative description of membrane current and its application to conduction and excitation in nerve. The J phys.Hubel & Wiesel (1962). Receptive fields, binocular interaction and functional architecture in the cat's visual cortex. The J phys.Lettvin... (1959). What the frog's eye tells the frog's brain. Proceedings of IRE.Miller (1956). The magical number seven, plus or minus two ... Psych Rev.O'Keefe & Dostrovsky (1971). The hippocampus as a spatial map ... Brain research.Omer ... (2018). Social place-cells in the bat hippocampus. Science.Sarel ... (2017). Vectorial representation of spatial goals in the hippocampus of bats. Science.Sarel ... (2022). Natural switches in behaviour rapidly modulate hippocampal coding. Nature.Tsoar ... (2011). Large-scale navigational map in a mammal. PNAS.Ulanovsky ... (2003). Processing of low-probability sounds by cortical neurons. Nature neuroscience.Ulanovsky & Moss (2007). Hippocampal cellular and network activity in freely moving echolocating bats. Nat Neuro.Yartsev & Ulanovsky (2013). Representation of three-dimensional space in the hippocampus of flying bats. Science.

References Nat Commun. 2022; 13: 4435. Nat Commun 2020; 11: 35 Hayward, J. 1971. "You Can Never Go Home" Moody Blues. https://youtu.be/mUhboF8d1x0?si=IX4iP_W0f3uR65qo Jagger, Richards, Oldham. 1964. "As Tears Go By". Marianne Faithful. https://youtu.be/S8EykQaZ8CU?si=X42TiNsveR7rwdHB --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support

Dans cet épisode, Mathilde revient sur ces idées qui circulent parfois, selon lesquelles il ne faut pas trop dépenser son chien ni le faire travailler. Au travers de publications scientifiques établies sur plusieurs espèces, on discute de l'idée que l'on peut ou non trop dépenser son chien. Références Roshanaei-Moghaddam, B., Katon, W. J., & Russo, J. (2009). The longitudinal effects of depression on physical activity. General hospital psychiatry, 31(4), 306-315. Nimmo, M. A., Leggate, M., Viana, J. L., & King, J. A. (2013). The effect of physical activity on mediators of inflammation. Diabetes, Obesity and Metabolism, 15(s3), 51-60. Albert, M. A., Glynn, R. J., & Ridker, P. M. (2004). Effect of physical activity on serum C-reactive protein. The American journal of cardiology, 93(2), 221-225. Neeper, S. A., Gómez-Pinilla, F., Choi, J., & Cotman, C. W. (1996). Physical activity increases mRNA for brain-derived neurotrophic factor and nerve growth factor in rat brain. Brain research, 726(1-2), 49-56. Sierakowiak, A., Mattsson, A., Gómez-Galán, M., Feminía, T., Graae, L., Aski, S. N., ... & Åberg, E. (2015). Hippocampal morphology in a rat model of depression: the effects of physical activity. The open neuroimaging journal, 9, 1. McGowan, R. T., Rehn, T., Norling, Y., & Keeling, L. J. (2014). Positive affect and learning: exploring the “Eureka Effect” in dogs. Animal cognition, 17, 577-587. Väätäjä, H., Majaranta, P., Cardó, A. V., Isokoski, P., Somppi, S., Vehkaoja, A., ... & Surakka, V. (2021). The Interplay Between Affect, Dog's Physical Activity and Dog–Owner Relationship. Frontiers in Veterinary Science, 8, 673407. Hintze, S., & Yee, J. R. (2021). Animals in flow–Towards the scientific study of intrinsic reward in animals. PsyArXiv.

Lynn Nadel is an emeritus professor at the University of Arizona, where his research focuses on the role of the hippocampus in memory. This is our second conversation. We discuss how the Hippocampus as a Cognitive Map was received, Lynn's career, including his years as head of department at the University of Arizona, how to foster collaboration, why Lynn started the Hippocampal History project, and the development and clinical aspects of the hippocampus.BJKS Podcast is a podcast about neuroscience, psychology, and anything vaguely related, hosted by Benjamin James Kuper-Smith.Support the show: https://geni.us/bjks-patreonTimestamps00:00: Who was A. Black?03:38: How was The Hippocampus as a Cognitive Map received?08:08: Lynn's wandering years15:46: At the University of Arizona21:24: How to foster collaboration28:29: Being a head of department38:22: The Hippocampal History project42:56: Lynn's developmental workPodcast linksWebsite: https://geni.us/bjks-podTwitter: https://geni.us/bjks-pod-twtLynn's linksWebsite: https://geni.us/nadel-webMastodon: https://geni.us/nadel-mastodonBen's linksWebsite: https://geni.us/bjks-webGoogle Scholar: https://geni.us/bjks-scholarTwitter: https://geni.us/bjks-twtReferencesLynn's first episode: https://geni.us/bjks-nadelBlack, Nadel & O'Keefe (1977). Hippocampal function in avoidance learning and punishment. Psychological Bulletin.Edgin, Spano, Kawa & Nadel (2014). Remembering things without context: development matters. Child development.Goddard (1964). Functions of the amygdala. Psychological bulletin.Lynch (1979). Representations in the Brain: The Hippocampus as a Cognitive Map. John O'Keefe and Lynn Nadel. Science.Nadel & Moscovitch (1997). Memory consolidation, retrograde amnesia and the hippocampal complex. Current opinion in neurobiology.Nadel, Samsonovich, Ryan & Moscovitch (2000). Multiple trace theory of human memory: computational, neuroimaging, and neuropsychological results. Hippocampus.Nadel, Willner & Kurz (1986). The neurobiology of mental representations. In Myles Brand (ed.), The Representation of Knowledge and Belief. Tucson: University of Arizona Press.O'Keefe & Nadel (1978) The Hippocampus as a Cognitive Map. Free download: https://discovery.ucl.ac.uk/id/eprint/10103569/O'Keefe & Nadel (1979). Précis of O'Keefe & Nadel's The hippocampus as a cognitive map. Behavioral and Brain Sciences.Pennington, Moon, Edgin, Stedron & Nadel (2003). The neuropsychology of Down syndrome: evidence for hippocampal dysfunction. Child development.Ravindran (2022). Profile of Lynn Nadel. PNAS. Squire, Nadel & Slater (1981). Anterograde amnesia and memory for temporal order. Neuropsychologia.Sutherland & Rudy (1989). Configural association theory: The role of the hippocampal formation in learning, memory, and amnesia. Psychobiology.

呼吸の状態によって記憶のしやすさが変わるという、 「その角度からくるのは予想してなかったわー」という論文を紹介しました。 　【プレスリリース】 呼吸パターンが記憶力の強化と悪化の両側面を引き起こすことを発見 https://www.hyo-med.ac.jp/corporation/publicity/news-releases/2043/ 【元論文】 Hippocampal ensemble dynamics and memory performance are modulated by respiration during encoding https://doi.org/10.1038/s41467-023-40139-7 いんよう！YouTubeチャンネル いんよう！Twitter いんよう！ブログ いんよう！文字起こし アーカイブ by Keiさん（本編の音声の文字起こしをnoteに上げてくれています）

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.08.01.551513v1?rss=1 Authors: de Haas, N., Ottink, L., Doeller, C. Abstract: The hippocampus is a key region for forming mental maps of our environment. These maps represent spatial information such as distances between landmarks. A cognitive map can allow for flexible inference of spatial relationships that have never been directly experienced before. Previous work has shown that the human hippocampus encodes distances between locations, but it is unclear how Euclidean and path distances are distinguished. In this study, participants performed an object-location task in a virtual environment. We combined functional magnetic resonance imaging with representational similarity analysis to test how Euclidean and path distances are represented in the hippocampus. We observe that hippocampal neural pattern similarity for objects scales with Euclidean as well as path distance between object locations, suggesting that the hippocampus integrates both types of distances. One key characteristic of cognitive maps is their adaptive and flexible nature. We therefore subsequently modified path distances between objects using roadblocks in the environment. We found that hippocampal pattern similarity between objects adapted as a function of these changes in path distance, selectively in egocentric navigators but not in allocentric navigators Taken together, our study supports the idea that the hippocampus creates integrative and flexible cognitive maps. 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/2023.08.03.551808v1?rss=1 Authors: Ribeiro, F. C., Cozachenco, D., Argyrousi, E. K., Staniszewski, A., Wiebe, S., Calixtro, J. D., Soares-Neto, R., Al-Chami, A., El Sayegh, F., Bermudez, S., Arsenault, E., Cossenza, M., Lacaille, J.-C., Nader, K., Sun, H., De Felice, F. G., Lourenco, M. V., Arancio, O., Aguilar-Valles, A., Sonenberg, N., Ferreira, S. T. Abstract: Impaired synaptic plasticity and progressive memory deficits are major hallmarks of Alzheimer's disease (AD). Hippocampal mRNA translation, required for memory consolidation, is defective in AD. Here, we show that genetic reduction of the translational repressors, Fragile X messenger ribonucleoprotein (FMRP) or eukaryotic initiation factor 4E (eIF4E)-binding protein 2 (4E-BP2), ameliorated the inhibition of hippocampal protein synthesis and memory impairment induced by AD-linked amyloid-b; oligomers (AbOs) in mice. Furthermore, systemic treatment with (2R,6R)-hydroxynorketamine (HNK), an active metabolite of the antidepressant ketamine, prevented deficits in hippocampal mRNA translation, long-term potentiation (LTP) and memory induced by AbOs in mice. HNK activated hippocampal signaling by extracellular signal-regulated kinase 1/2 (ERK1/2), mechanistic target of rapamycin (mTOR), and p70S6 kinase 1 (S6K1)/ribosomal protein S6 (S6), which promote protein synthesis and synaptic plasticity. S6 phosphorylation instigated by HNK was mediated by mTOR in hippocampal slices, while rescue of hippocampal LTP and memory in HNK-treated AbO-infused mice depended on ERK1/2 and, partially, on mTORC1. Remarkably, treatment with HNK corrected LTP and memory deficits in aged APP/PS1 mice. RNAseq analysis showed that HNK reversed aberrant signaling pathways that are upregulated in APP/PS1 mice, including inflammatory and hormonal responses and programmed cell death. Taken together, our findings demonstrate that upregulation of mRNA translation corrects deficits in hippocampal synaptic plasticity and memory in AD models. The results raise the prospect that HNK could serve as a therapeutic to reverse memory decline in AD. 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/2023.07.28.550946v1?rss=1 Authors: Masoliver, M., Davidsen, J., Nicola, W. Abstract: The 8-12 Hz theta rhythm observed in hippocampal local field potentials of animals can be regarded as a 'clock' that regulates the timing of spikes. While different interneuron sub-types synchronously phase lock to different phases for every theta cycle, the phase of pyramidal neurons' spikes asynchronously vary in each theta cycle, depending on the animal's position. On the other hand, pyramidal neurons tend to fire slightly faster than the theta oscillation in what is termed hippocampal phase precession. Chimera states are specific solutions to dynamical systems where synchrony and asynchrony coexist, similar to the hippocampal theta oscillation. Here, we test the hypothesis that the hippocampal theta oscillation emerges from chimera dynamics with computational modelling. We utilized multiple network topologies and sizes of Kuramoto oscillator networks that are known to collectively display chimera dynamics. We found that by changing the oscillators' intrinsic frequency, the frequency ratio between the synchronized and unsynchronized oscillators can match the frequency ratio between the hippocampal theta oscillation (approximately 8 Hz) and phase precessing pyramidal neurons (approximately 9 Hz). The faster firing population of oscillators also displays theta-sequence-like behaviour and phase precession. Finally, we trained networks of spiking integrate-and-fire neurons to output a chimera state by using the Kuramoto-chimera system as a dynamical supervisor. We found that the firing times of subsets of individual neurons display phase precession. These results imply that the hippocampal theta oscillation may be a chimera state, further suggesting the importance of chimera states in neuroscience. 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/2023.07.27.550869v1?rss=1 Authors: Heuer, S. E., Nickerson, E. W., Howell, G. R., Bloss, E. B. Abstract: The disconnection of neuronal circuits through synaptic loss is presumed to be a major driver of age-related cognitive decline. Age-related cognitive decline is heterogeneous, yet whether genetic mechanisms differentiate successful from unsuccessful cognitive decline through synaptic structural mechanisms remains unknown. Previous work using rodent and primate models leveraged various techniques to suggest that age-related synaptic loss is widespread on pyramidal cells in prefrontal cortex (PFC) circuits but absent on those in area CA1 of the hippocampus. Here, we examined the effect of aging on synapses on projection neurons forming a hippocampal-cortico-thalamic circuit important for spatial working memory tasks from two genetically distinct mouse strains that exhibit susceptibility (C57BL/6J) or resistance (PWK/PhJ) to cognitive decline during aging. Across both strains, synapses on the CA1-to-PFC projection neurons appeared completely intact with age. In contrast, we found synapse loss on PFC-to-nucleus reuniens (RE) projection neurons from aged C57BL/6J but not PWK/PhJ mice. Moreover, synapses from aged PWK/PhJ mice but not from C57BL/6J exhibited morphological changes that suggest increased synaptic efficiency to depolarize the parent dendrite. Our findings suggest resistance to age-related cognitive decline results in part by age-related synaptic adaptations, and identification of these mechanisms in PWK/PhJ mice could uncover new therapeutic targets for promoting successful cognitive aging and extending human health span. 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/2023.07.27.550892v1?rss=1 Authors: Montagrin, A., Croote, D. E., Preti, M. G., Lerman, L., Baxter, M. G., Schiller, D. Abstract: Our brain must manage multiple goals that differ in their temporal proximity. Some goals require immediate attention, while others have already been accomplished, or will be relevant later in time. Here, we examined how the hippocampus represents the temporal distance to different goals using a novel space-themed paradigm during 7T functional MRI (n=31). The hippocampus has an established role in mental time travel and a system in place to stratify information along its longitudinal axis on the basis of representational granularity. Previous work has documented a functional transformation from fine-grained, detail rich representations in the posterior hippocampus to coarse, gist-like representations in the anterior hippocampus. We tested whether the hippocampus uses this long axis system to dissociate goals based upon their temporal distance from the present. We hypothesized that the hippocampus would distinguish goals relevant for ones current needs from those that are removed in time along the long axis, with temporally removed past and future goals eliciting increasingly anterior activation. We sent participants on a mission to Mars where they had to track goals that differed in when they needed to be accomplished. We observed a long-axis dissociation, where temporally removed past and future goals activated the left anterior hippocampus and current goals activated the left posterior hippocampus. Altogether, this study demonstrates that the timestamp attached to a goal is a key driver in where the goal is represented in the hippocampus. This work extends the scope of the hippocampus long axis system to the goal-mapping domain. 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/2023.07.22.550041v1?rss=1 Authors: Paul, D., Srivastava, A., Banerjee, J., Tripathi, M., Doddamani, R., Lalwani, S., Siraj, F., Sharma, M. C., Chandra, P. S., Dixit, A. Abstract: Inflammation and blood brain barrier (BBB) damage are associated with epileptogenesis in Mesial Temporal lobe epilepsy with Hippocampal sclerosis (MTLE-HS). Animal studies have predicted the role of Matrix metalloproteinase 9 (MMP9) in extracellular matrix (ECM) modulation, BBB leakage and neuro-inflammation, while Transforming growth factor beta (TGF{beta}) signalling in astrocytes potentiates hyper-excitability leading to seizure generation. We hypothesize whether changes in activity and expression of MMP9, and the ratio of MMP9 and its inhibitor, Tissue inhibitor of metalloproteinase 1 (TIMP1), have a role in epileptogenesis in the patients with MTLE-HS through zona occludens 1 (ZO1) modulation. We also proposed the role of astrocytic TGF{beta} signalling in these patients. mRNA expression of MMP9 and TIMP1 was significantly up-regulated. The ratio of MMP9 to its inhibitor TIMP1 was greater than one, suggesting activation of MMP9, further confirmed by gelatin zymography. MMP9 activity as well as immunoreactivity was higher in patients with MTLE-HS as compared to non-seizure controls, whereas the immunoreactivity of ZO1 was significantly lower in the patients. The downstream TGF{beta} signalling effector molecules, SMAD3 and pSMAD3 immunoreactivity were also significantly higher in MTLE-HS patients and both molecules showed co-localisation with astrocytes in the hippocampal region. Further, we showed preliminary data about interaction of MMP9 and TGF{beta}1 in these patients as evidenced by a co-immunoprecipitation assay. This study highlighted the MMP9 and astrocytic TGF{beta} signalling mediated potential mechanism of epileptogenesis in MTLE-HS patients. 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/2023.07.19.549533v1?rss=1 Authors: Haast, R. A., Kashyap, S., Ivanov, D., Yousif, M. D., DeKraker, J., Poser, B. A., Khan, A. R. Abstract: We present a comprehensive study on the non-invasive measurement of hippocampal perfusion. Using high-resolution 7 Tesla arterial spin labelling data, we generated robust perfusion maps and observed significant variations in perfusion among hippocampal subfields, with CA1 exhibiting the lowest perfusion levels. Notably, these perfusion differences were robust and detectable even within five minutes and just fifty perfusion-weighted images per subject. To understand the underlying factors, we examined the influence of image quality metrics, various tissue microstructure and morphometry properties, macrovasculature and cytoarchitecture. We observed higher perfusion in regions located closer to arteries, demonstrating the influence of vascular proximity on hippocampal perfusion. Moreover, ex vivo cytoarchitectonic features based on neuronal density differences appeared to correlate stronger with hippocampal perfusion than morphometric measures like gray matter thickness. These findings emphasize the interplay between microvasculature, macrovasculature, and metabolic demand in shaping hippocampal perfusion. Our study expands the current understanding of hippocampal physiology and its relevance to neurological disorders. By providing in vivo evidence of perfusion differences between hippocampal subfields, our findings have implications for diagnosis and potential therapeutic interventions. In conclusion, our study provides a valuable resource for extensively characterising hippocampal perfusion. 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/2023.07.19.549725v1?rss=1 Authors: Parkins, E. V., Brager, D. H., Rymer, J. K., Burwinkel, J. M., Rojas, D., Tiwari, D., Hu, Y.-C., Gross, C. Abstract: MicroRNAs are an emerging class of synaptic regulators. These small noncoding RNAs post-transcriptionally regulate gene expression, thereby altering neuronal pathways and shaping cell-to-cell communication. Their ability to rapidly alter gene expression and target multiple pathways makes them interesting candidates in the study of synaptic plasticity. Here, we demonstrate that the proconvulsive microRNA miR-324-5p regulates excitatory synapse structure and function in the hippocampus of mice. Both Mir324 knockout (KO) and miR-324-5p antagomir treatment significantly reduce dendritic spine density in the hippocampal CA1 subregion, and Mir324 KO, but not miR-324-5p antagomir treatment, shift dendritic spine morphology, reducing the proportion of thin, 'unstable' spines. Western blot and quantitative Real-Time PCR revealed changes in protein and mRNA levels for potassium channels, cytoskeletal components, and synaptic markers, including MAP2 and Kv4.2, which are essential for long-term potentiation (LTP). In line with these findings, slice electrophysiology revealed that LTP is severely impaired in Mir324 KO mice, while baseline excitatory activity remains unchanged. Overall, this study demonstrates that miR-324-5p regulates dendritic spine density, morphology, and plasticity in the hippocampus, potentially via multiple cytoskeletal and synaptic modulators. 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/2023.07.14.549070v1?rss=1 Authors: Martinez, J. D., Wilson, L. G., Brancaleone, W., Peterson, K., Popke, D. S., Caicedo Garzon, V., Perez Tremble, R., Donnelly, M. J., Mendez Ortega, S., Torres, D., Shaver, J., Clawson, B. C., Jiang, S., Yang, Z., Aton, S. Abstract: Fragile X syndrome (FXS) is a highly-prevalent genetic cause of intellectual disability, associated with disrupted cognition and sleep abnormalities. Sleep loss itself negatively impacts cognitive function, yet the contribution of sleep loss to impaired cognition in FXS is vastly understudied. One untested possibility is that disrupted cognition in FXS is exacerbated by abnormal sleep. We hypothesized that restoration of sleep-dependent mechanisms could improve functions such as memory consolidation in FXS. We examined whether administration of ML297, a hypnotic drug acting on G-protein-activated inward-rectifying potassium channels, could restore sleep phenotypes and improve disrupted memory consolidation in Fmr1-/y mice. Using 24-h polysomnographic recordings, we found that Fmr1-/y mice exhibit reduced non-rapid eye movement (NREM) sleep and fragmented NREM sleep architecture, alterations in NREM EEG spectral power (including reductions in sleep spindles), and reduced EEG coherence between cortical areas. These alterations were reversed in the hours following ML297 administration. Hypnotic treatment following contextual fear or spatial learning also ameliorated disrupted memory consolidation in Fmr1-/y mice. Hippocampal activation patterns during memory recall was altered in Fmr1-/y mice, reflecting an altered balance of activity among principal neurons vs. parvalbumin-expressing (PV+) interneurons. This phenotype was partially reversed by post-learning ML297 administration. These studies suggest that sleep disruption could have a major impact on neurophysiological and behavioral phenotypes in FXS, and that hypnotic therapy may significantly improve disrupted cognition in this disorder. 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/2023.07.10.547981v1?rss=1 Authors: Arndt, K. C., Gilbert, E. T., Klaver, L. M. F., Kim, J., Buhler, C. M., Basso, J. C., McKenzie, S. A., English, D. F. Abstract: Neuronal oscillations support information transfer by temporally aligning the activity of anatomically distributed 'writer' and 'reader' cell assemblies. High-frequency oscillations (HFOs) such as hippocampal CA1 sharp-wave ripples (SWRs; 100-250 Hz) are sufficiently fast to initiate synaptic plasticity between assemblies and are required for memory consolidation. HFOs are observed in parietal and midline cortices including granular retrosplenial cortex (gRSC). In offline brain states (e.g. quiet wakefulness) gRSC HFOs co-occur with CA1 SWRs, while in online states (e.g. ambulation) HFOs persist with the emergence of theta oscillations. The mechanisms of gRSC HFO oscillations, specifically whether the gRSC can intrinsically generate HFOs, and which layers support HFOs across states, remain unclear. We addressed these issues in behaving mice using optogenetic excitation in individual layers of the gRSC and high density silicon-probe recordings across gRSC layers and hippocampus CA1. Optogenetically induced HFOs (iHFOs) could be elicited by depolarizing excitatory neurons with 100 ms half-sine wave pulses in layer 2/3 (L2/3) or layer 5 (L5) though L5 iHFOs were of lower power than in L2/3. Critically, spontaneous HFOs were only observed in L2/3 and never in L5. Intra-laminar monosynaptic connectivity between excitatory and inhibitory neurons was similar across layers, suggesting other factors restrict HFOs to L2/3. To compare HFOs in online versus offline states we analyzed, separately, HFOs that did or did not co-occur with CA1 SWRs. Using current-source density analysis we found uniform synaptic inputs to L2/3 during all gRSC HFOs, suggesting layer-specific inputs may dictate the localization of HFOs to L2/3. HFOs occurring without SWRs were aligned with the descending phase of both gRSC and CA1 theta oscillations and were coherent with CA1 high frequency gamma oscillations (50-80 Hz). These results demonstrate that gRSC can internally generate HFOs without rhythmic inputs and that HFOs occur exclusively in L2/3, coupled to distinct hippocampal oscillations in online versus offline states. 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/2023.07.10.548388v1?rss=1 Authors: Jiang, H., Cai, J., Santos-Pata, D., Shi, L., Zhu, X., Tong, J., Cai, Y., Li, C., Wang, R., Yin, J., Zhang, S., Kwok, S. C. Abstract: Navigating within our neighborhood, learning a set of concepts, or memorizing a story, requires remembering the relationship between individual items that are presented sequentially. Theta activity in the mammalian hippocampus has been related to the encoding and recall of relational structures embedding episodic memories. However, how theta oscillations are involved in retrieving temporal order information in opposing directionality (forward vs backward) has not been characterized. Here, using intracranial recordings from 10 human epileptic patients of both genders with hippocampal electrodes, we tested the patients with a temporal order memory task in which they learned the spatial relationship among individual items arranged along a circular track and were tested on both forward-cued and backward-cued retrieval conditions. We found that sustained high-power oscillatory events in the hippocampal theta (2-8 Hz) band, as quantified by Pepisode rate, were higher for the backward conditions during the later stage but not in the earlier stage. The theta Pepisode results are consistent with the behavioral memory performance. In contrast, we observed a stronger effect of forward than backward retrieval for the gamma (30-70 Hz) Pepisode rate irrespective of stages. Our results revealed differential roles of theta vs. gamma oscillations in the retrieval of temporal order and how theta oscillations are specifically implicated in the learning process for efficient retrieval of temporal order memories under opposing directionality. 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/2023.07.07.548060v1?rss=1 Authors: Maheshwari, M., Singla, A., Rawat, A., Banerjee, T., Pati, S., Shah, S., Maiti, S., Vaidya, V. A. Abstract: Adult hippocampal neurogenesis is a lifelong process that involves the integration of newborn neurons into the hippocampal network, and plays a role in cognitive function and the modulation of mood-related behavior. Here, we sought to address the impact of chemogenetic activation of adult hippocampal progenitors on distinct stages of progenitor development, including quiescent stem cell activation, progenitor turnover, differentiation and morphological maturation. We find that hM3Dq-DREADD-mediated activation of nestin-positive adult hippocampal progenitors recruits quiescent stem cells, enhances progenitor proliferation, increases doublecortin-positive newborn neuron number, accompanied by an acceleration of differentiation and morphological maturation, associated with increased dendritic complexity. Behavioral analysis indicated anxiolytic behavioral responses in transgenic mice subjected to chemogenetic activation of adult hippocampal progenitors at time-points when newborn neurons are predicted to integrate into the mature hippocampal network. Furthermore, we noted an enhanced fear memory extinction on a contextual fear memory learning task in transgenic mice subjected to chemogenetic activation of adult hippocampal progenitors. Our findings indicate that hM3Dq-DREAD-mediated chemogenetic activation of adult hippocampal progenitors impacts distinct aspects of hippocampal neurogenesis, associated with the regulation of anxiety-like behavior and fear memory extinction. 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/2023.06.26.546556v1?rss=1 Authors: Hanssen, K. S., Winter-Hjelm, N., Niethammer, S. N., Kobro-Flatmoen, A., Witter, M. P., Sandvig, A., Sandvig, I. Abstract: Engineered biological neural networks are indispensable tools for investigating neural function in both healthy and diseased states from the subcellular to the network level. Neurons in vitro self-organize over time into networks of increasing structural and functional complexity, thus maintaining emergent dynamics of neurons in the brain. While in vitro neural network model systems have advanced significantly over the past decade, there is still a need for models able to recapitulate topological and functional organization of brain networks. Especially relevant in this context are interfaces which can support the establishment of multinodal interconnected networks of different neural populations, which at the same time enable control of the direction of connectivity between the nodes. An added required feature of such interfaces is compatibility with electrophysiological techniques and optical imaging tools to facilitate studies of neural network structure-function dynamics. In this study, we applied a custom-designed microfluidic device with Tesla-valve inspired microchannels for structuring multinodal neural networks with controllable feedforward connectivity between rat primary cortical and hippocampal neurons. By interfacing these devices with nanoporous microelectrode arrays, we demonstrate how both spontaneously evoked and stimulation induced activity propagates, as intended, in a feedforward pattern between the different interconnected neural nodes. Moreover, we show that these multinodal networks exhibit functional dynamics suggestive of capacity for both segregated and integrated activity. To advocate the broader applicability of this model system, we also provide proof of concept of long-term culturing of subregion- and layer specific neurons extracted from the entorhinal cortex and hippocampus of adult Alzheimers-model mice and rats. We show that these neurons re-form structural connections and develop spontaneous spiking activity after 15 days in vitro. Our results thus highlight the suitability and potential of our approach for reverse engineering of biologically and anatomically relevant multinodal neural networks supporting the study of dynamic structure-function relationships in both healthy and pathological conditions. 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/2023.06.23.546219v1?rss=1 Authors: Iwata, T., Yanagisawa, T., Ikegaya, Y., Smallwood, J., Fukuma, R., Oshino, S., Tani, N., Khoo, H. M., Kishima, H. Abstract: Core features of human cognition, for example, the experience of mind wandering, highlight the importance of the capacity to focus on information separate from the here and now. However, the brain mechanisms that underpin these self-generated states remain unclear. An emerging hypothesis is that self-generated states depend on the process of memory replay, which, in animals, is linked to sharp-wave ripples (SWRs) originating in the hippocampus. SWRs are transient high-frequency oscillations that exhibit circadian fluctuations and, in the laboratory, are important for memory and planning. Local field potentials were recorded from the hippocampus of 11 patients with epilepsy for up to 15 days, and experience sampling was used to describe their association with ongoing thought patterns. SWRs were correlated with patterns of vivid, intrusive ongoing thoughts unrelated to the task being performed, establishing their contribution to the ongoing thoughts that humans experience in daily life. 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/2023.06.24.546401v1?rss=1 Authors: Joy, M. S. H., Nall, D. L., Emon, B., Lee, K. Y., Barishman, A., Ahmed, M., Rahman, S., Selvin, P. R., Saif, M. T. A. Abstract: Neurons in the brain communicate with each other at their synapses. It has long been understood that this communication occurs through biochemical processes. Here, we reveal a previously unrecognized paradigm wherein mechanical tension in neurons is essential for communication. Using in vitro rat hippocampal neurons, we find that (1) neurons become tout/tensed after forming synapses resulting in a contractile neural network, and (2) without this contractility, neurons fail to fire. To measure time evolution of network contractility in 3D (not 2D) extracellular matrix, we developed an ultra-sensitive force sensor with 1 nN resolution. We employed Multi-Electrode Array (MEA) and iGluSnFR, a glutamate sensor, to quantify neuronal firing at the network and at the single synapse scale, respectively. When neuron contractility is relaxed, both techniques show significantly reduced firing. Firing resumes when contractility is restored. Neural contractility may play a crucial role in memory, learning, cognition, and various neuropathologies. 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

Twins Dani Bassett and Perry Zurn are curious. Their work, individually and together, gives new conception and language to what curiosity is, the work that it does in the world. These are human beings of intelligence and integrity and deep care, and their reification of curiosity might just be a generative narrative of our time.  Origins Podcast WebsiteFlourishing Commons NewsletterShow Notes:Homeschooling (05:00)Epistemology (09:00)multiple discovery (16:30)foregrounding bravery (21:00)Curious Minds(25:00)Julio Ottino on Origins (28:30)Hope in the Dark by Rebecca Solnit (32:00)Power of curiosity for social movements (34:30)Three types of curiosity (40:30)David Lydon-Staley University of Pennsylvania (44:00)Cognitive flexibility and the discovery of neuroplasticity (45:30)Talking to Strangers by Danielle Allen (47:00)Amartya Sen - democracy is a knowledge and a process of social discovery (53:00)How thought moves (54:00)Dani's course 'the goals of scientific inquiry (55:15)Hippocampal system and mapping conceptual spaces (56:30)Networks as the lingua franca of complex systems (58:00)Lightning round (59:00)Book: Dani - Follow My Leader by and A Room of One's Own by Virginia Wolff; Perry - Alice in Wonderland by Lewis Carroll and books that make him slow downSusan Sontag 'I no longer trust novels which fully satisfy my passion to understand.'Passion: Perry - methods, ways of asking questions; Dani - analogical powerHeart Sing: Dani - Spring; Perry - punctuation marksOn Earth We're Briefly Gorgeous by Ocean Vuong Screwed up: Dani - leaving nursing school; Perry - some breakupsFind Dani online:WebsiteTwitter: @DaniSBassettFind Perry online:WebsiteTwitter: @perryzurn'Five-Cut Fridays' five-song music playlist series  Dani and Perry's playlistLogo artwork by Cristina GonzalezMusic by swelo on all streaming platforms or @swelomusic on social media

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.05.05.539468v1?rss=1 Authors: Gulfo, M. C., Lebowitz, J. J., Ramos, C., Hwang, D.-W., Nasrallah, K., Castillo, P. E. Abstract: Hilar mossy cells (MCs) are principal excitatory neurons of the dentate gyrus (DG) that play critical roles in hippocampal function and have been implicated in brain disorders such as anxiety and epilepsy. However, the mechanisms by which MCs contribute to DG function and disease are poorly understood. Expression from the dopamine D2 receptor (D2R) gene (Drd2) promoter is a defining feature of MCs, and previous work indicates a key role for dopaminergic signaling in the DG. Additionally, the involvement of D2R signaling in cognition and neuropsychiatric conditions is well-known. Surprisingly, though, the function of MC D2Rs remain largely unexplored. In this study, we show that selective and conditional removal of Drd2 from MCs of adult mice impaired spatial memory, promoted anxiety-like behavior and was proconvulsant. To determine the subcellular expression of D2Rs in MCs, we used a D2R knockin mouse which revealed that D2Rs are enriched in the inner molecular layer of the DG, where MCs establish synaptic contacts with granule cells. D2R activation by exogenous and endogenous dopamine reduced MC to dentate granule cells (GC) synaptic transmission, most likely by a presynaptic mechanism. In contrast, removing Drd2 from MCs had no significant impact on MC excitatory inputs and passive and active properties. Our findings support that MC D2Rs are essential for proper DG function by reducing MC excitatory drive onto GCs. Lastly, impairment of MC D2R signaling could promote anxiety and epilepsy, therefore highlighting a potential therapeutic target. 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/2023.05.05.539539v1?rss=1 Authors: Contreras, A., Djebari, S., Temprano, S., Munera, A., Gruart, A. D., Delgado-Garcia, J. M., Jimenez-Diaz, L., Navarro-Lopez, J. D. Abstract: Learning and memory occurrence requires of hippocampal long-term synaptic plasticity and a precise neural activity orchestrated by brain network oscillations, both processes reciprocally influencing each other. As G protein-gated inwardly rectifying potassium (GIRK) channels rule synaptic plasticity that supports hippocampal dependent memory, here we assessed their unknown role in hippocampal oscillatory activity in relation to synaptic plasticity induction. In alert male mice, pharmacological GIRK modulation did not alter neural oscillations before long-term potentiation (LTP) induction. However, after an LTP generating protocol, both gain- and loss of basal GIRK activity transformed LTP into long-term depression, but only specific suppression of constitutive GIRK activity caused a disruption of network synchronization (delta, alpha, gamma bands), even leading to long-lasting ripples and fast ripples pathological oscillations. Together, our data showed that constitutive GIRK activity plays a key role in the tuning mechanism of hippocampal oscillatory activity during long-term synaptic plasticity processes that underlies hippocampal-dependent cognitive functions. 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/2023.05.03.539225v1?rss=1 Authors: Calatayud-Baselga, I., Casares-Crespo, L., Franch-Ibanez, C., Guijarro-Nuez, J., Sanz, P., Mira, H. Abstract: 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/2023.05.03.539307v1?rss=1 Authors: Zong, W., Zhou, J., Gardner, M. P. H., Costa, K. M., Zhang, Z., Schoenbaum, G. Abstract: The orbitofrontal cortex (OFC) and hippocampus (HC) are both implicated in the formation of cognitive maps and their generalization into schemas, which reflect the components and relationships that define the world around us. However how these areas interact in supporting this global function remains an open question, with some proposals supporting a serial model in which hippocampus constructs task representations which orbitofrontal cortex draws upon to extract key behavioral features and others proposing a parallel model in which both regions construct task representations that highlight different types of information, like layers on a map. Here we tested between these two models by asking how schema correlates in orbitofrontal cells would be affected by inactivation of hippocampal output during performance and transfer across problems in an odor-based virtual figure 8 maze task. We found the prevalence and content of schema correlates were unaffected by hippocampal inactivation after learning of a new problem, while inactivation during learning accelerated their formation. These results are contrary to a serial model in which OFC depends on hippocampal output and strongly favor the proposal that OFC and HC operate in parallel to extract different features defining cognitive maps and schemas. 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/2023.05.02.539011v1?rss=1 Authors: Simard, S., Rahimian, R., Davoli, M. A., Theberge, S., Matosin, N., Turecki, G., Nagy, C., Mechawar, N. Abstract: 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/2023.05.01.538923v1?rss=1 Authors: Viana, J. F., Guerra-Gomes, S., Abreu, D. S., Machado, J. L., Barsanti, S., Goncalves, M., Martin-Monteagudo, C., Sardinha, V., Nascimento, D., Tavares, G., Irmler, M., Beckers, J., Korostynski, M., Sousa, N., Navarrete, M., Teixeira-Castro, A., Pinto, L., Oliveira, J. F. Abstract: 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/2023.05.01.538951v1?rss=1 Authors: Baumgartner, N. E., Biraud, M. C., Lucas, E. K. Abstract: 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/2023.04.24.538047v1?rss=1 Authors: Hood, R. J., Sanchez Bezanilla, S., Beard, D. J., Rust, R., Turner, R. J., Stuckey, S. M., Collins-Praino, L. E., Walker, F. R., Nilsson, M., Ong, L. K. Abstract: 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/2023.04.28.538785v1?rss=1 Authors: Watanabe, Y., Ikegaya, Y., Yanagisawa, T. Abstract: 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/2023.04.27.538595v1?rss=1 Authors: Nguyen, R., Sivakumaran, S., Lambe, E. K., Kim, J. Abstract: Associating contexts with rewards depends on hippocampal circuits, with local inhibitory interneurons positioned to play an important role in shaping activity. Here, we hypothesize that the encoding of context-reward memory requires a ventral hippocampus (vHPC) to nucleus accumbens (NAc) circuit that is gated by CCK interneurons. In a sucrose conditioned place preference (CPP) task, optogenetically inhibiting vHPC-NAc terminals impaired the acquisition of place preference. Transsynaptic rabies tracing revealed vHPC-NAc neurons were monosynaptically innervated by CCK interneurons. Using intersectional genetic targeting of CCK interneurons, ex vivo optogenetic activation of CCK interneurons increased GABAergic transmission onto vHPC-NAc neurons, while in vivo optogenetic inhibition of CCK interneurons increased cFos in these neurons. Notably, CCK interneuron inhibition during sucrose CPP learning increased time spent in the sucrose-associated location, suggesting enhanced place-reward memory. Our findings reveal a previously unknown hippocampal microcircuit crucial for modulating the strength of contextual reward learning. 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/2023.04.27.538511v1?rss=1 Authors: Chamberland, S., Grant, G., Machold, R. P., Nebet, E. R., Tian, G., Hanani, M., Kullander, K., Tsien, R. W. Abstract: Hippocampal somatostatin-expressing (Sst) GABAergic interneurons (INs) exhibit considerable anatomical and functional heterogeneity. Recent single cell transcriptome analyses have provided a comprehensive Sst-IN subtype census, a plausible molecular ground truth of neuronal identity whose links to specific functionality remain incomplete. Here, we designed an approach to identify and access subpopulations of Sst-INs based on transcriptomic features. Four mouse models based on single or combinatorial Cre- and Flp- expression differentiated functionally distinct subpopulations of CA1 hippocampal Sst-INs that largely tiled the morpho-functional parameter space of the Sst-INs superfamily. Notably, the Sst;;Tac1 intersection revealed a population of bistratified INs that preferentially synapsed onto fast-spiking interneurons (FS-INs) and were both necessary and sufficient to interrupt their firing. In contrast, the Ndnf;;Nkx2-1 intersection identified a population of oriens lacunosum-moleculare (OLM) INs that predominantly targeted CA1 pyramidal neurons, avoiding FS-INs. Overall, our results provide a framework to translate neuronal transcriptomic identity into discrete functional subtypes that capture the diverse specializations of hippocampal Sst-INs. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Today on the Mushroom Hour Podcast we are blessed to speak with Manoj Doss. Manoj is a cognitive neuropsychopharmacologist at the Center for Psychedelic and Consciousness Research at Johns Hopkins University. His research is at the intersection of cognitive neuroscience and neuropsychopharmacology with focuses on episodic memory and hallucinogenic drugs. Manoj utilizes complex cognitive paradigms, brain imaging, and computational modelling to explore what makes psychedelics unique compared to other classes of psychoactive drugs, both in terms of basic drug effects and mechanisms for treating clinical populations. Although Manoj is optimistic that psychedelics will soon have a place in psychiatry, he remains cautious of exaggerated claims and negligence to potential downsides, something he terms 'psychedelic myopia'.    TOPICS COVERED:   Cognitive Neuroscience & Neuropsychopharmacology   Psychedelic Neuroscience   Types of Memory - Episodic, Semantic, Procedural   Parts of the Brain - Hippocampus, Neocortex   Recollection vs Familiarity   Psychedelics Impacting Memory through Familiarity   Is Memory Stored in Parts of the Body Other than the Brain?   How Do We Make False Memories?   Debunking the “Default Mode Network” Narrative   Psychedelic Science and Incorporating Existing Scientific Disciplines   Showing Psychedelics are Actually Useful in Treating Any Disorders   Commentary on Structuring Psychedelic Research   Future of Psychedelic Therapy as Adjunct to Existing Therapies?   Tempering Conclusions and Expectations from Psychedelic Research   EPISODE RESOURCES:   Manoj Doss Twitter: https://twitter.com/ManojDoss   Manoj Doss Researchgate: https://www.researchgate.net/profile/Manoj-Doss   Manoj Doss @ Johns Hopkins: https://hopkinspsychedelic.org/doss   John O'Keefe Nobel Prize work on Hippocampal place cells: https://www.nature.com/articles/s41586-022-04913-9   Doss et al paper on reward dynamics: http://dml.ucdavis.edu/uploads/6/1/9/7/61974117/gruber_ritchey_wang_doss_ranganath_2016.pdf   Default Mode Network Hypothesis: https://www.frontiersin.org/articles/10.3389/fnhum.2014.00020/full   PiHKAL: A Chemical Love Story by Alexander Shulgin: https://www.amazon.com/Pihkal-Chemical-Story-Alexander-Shulgin/dp/0963009605   Janice Chen paper on shared experience: https://scholar.google.com/citations?view_op=view_citation&hl=en&user=mOwF8UEAAAAJ&citation_for_view=mOwF8UEAAAAJ:M05iB0D1s5AC   Marc Berman paper on benefits of interacting with nature: https://journals.sagepub.com/doi/10.1111/j.1467-9280.2008.02225.x   

Welcome to the 9th episode of The Brain Podcast - the official podcast of the journals Brain and Brain Communications. In this episode we chat with Professor Robyn S. Klein, senior author of the article entitled: COVID-19 induces CNS cytokine expression and loss of hippocampal neurogenesis This article explores the ongoing challenge to better understand the mechanisms underlying the cognitive and neuropsychiatric sequlae of the Sars-CoV2 infection. We discuss the use of both animal model experiments and human post-mortem tissue investigation to gain insight on this topical condition. Check out the full article on the Brain website: https://doi.org/10.1093/brain/awac270 This episode was hosted, edited and produced by Xin You Tai; co-hosted by Sarosh Irani; co-produced by Joanne Bell; original music by Ammar Al-Chalabi.

What effect does marijuana have on the brain itself and the chemical activity happening at the neuron receptor sites? Over the last 10+ years smoking marijuana has become a widely accepted drug used recreationally and prescribed by doctors in some cases. It has become big business. But no one seems to be talking about the negative implications attached to using this carcinogenic drug that is highly addictive, is as harmful as tobacco and has long term impact on the brain, especially on younger developing brains. Internal medicine physician Dr. Annette Bosworth (Dr. Boz) returns to the Strong By Design podcast show to speak with host Chris Wilson about her scientifically backed research. This conversation is based on a recent 90-minute webinar she made showcasing the consequences of chronic marijuana use.   “Marijuana is a great example of how just compartmentalizing one organ would leave you missing the bigger punch line of what this molecule really does to the development of proper human, and the healing that people really want it to do but the evidence is not there.” -- Dr. Boz - Annette Bosworth   Time Stamps 00:28 - Welcome to the 'Strong By Design' podcast 03:48 - Meet today's special guest, Dr. Boz  07:02 - Dr. Boz gets real about marijuana and its effect on brain health 20:43 - Marijuana use among youth: Is it safe? 27:03 - Hippocampal growth: Dr. Boz on why it's crucial to educate teens about marijuana 34:55 - Discover other factors associated with blunted development of hippocampus  41:33 - Dr. Boz on hippocampus damage, and how to heal injured brains 44:04 - Learn how marijuana impacts the cannabinoid receptors of the brain 50:48 - How long does marijuana stay in your brain?   Resources: Dr Boz Webinar – Marijuana and Brain Health   Connect w/ Dr. Boz: Facebook Instagram YouTube   Connect w/ CriticalBench:  Youtube Facebook Instagram CriticalBench.com StrongByDesignPodcast.com

References Respir Res. 2017 Sep 6;18(1):168 Front Behav Neurosci. 2020; 14: 24 JLR Methods| 2020.Volume 61, ISSUE 11, P1512-1523, November 01 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message

Leila Reddy discusses her paper, “Human Hippocampal Neurons Track Moments in a Sequence of Events,” published in Vol. 41, Issue 31 of The Journal of Neuroscience, with Editor-in-Chief Marina Picciotto. Find our upcoming webinar schedule here. With special guest: Leila Reddy Hosted by: Marina Picciotto On Neuro Current, we delve into the stories and conversations surrounding research published in the journals of the Society for Neuroscience. Through its publications, JNeurosci, eNeuro, and the History of Neuroscience in Autobiography, SfN promotes discussion, debate, and reflection on the nature of scientific discovery, to advance the understanding of the brain and the nervous system.  Find out more about SfN and connect with us on Twitter, Instagram, and LinkedIn.  

How does our brain organize memories to plan future behaviour? In this episode, I feature a paper by Shahbaba and colleagues who leveraged complex behavioural and statistical machine learning approaches to uncover the fundamental mechanisms by which our brain organizes memories into sequences. This research constitutes a critical early step in understanding memory failure in cognitive disorders such as Alzheimer's disease and other forms of dementia.    Full citation: Shahbaba, B., Li, L., Agostinelli, F., Saraf, M., Cooper, K. W., Haghverdian, D., ... & Fortin, N. J. (2022). Hippocampal ensembles represent sequential relationships among an extended sequence of nonspatial events. Nature communications, 13(1), 1-17.

Soutenir et s'abonner à Neurosapiens Le sujet de cette semaine a été une évidence quand j'observe mon quotidien de nomade. Chaque semaine nous nous déplaçons de villes en villes en Amérique Latine et chaque semaine nous devons découvrir de nouvelles rues, de nouveaux espaces, de nouvelles directions. Comme le quotidien m'inspire beaucoup pour les épisodes de Neurosapiens, je me demande toujours dans ces moments-là s'il y a des prédispositions dans le cerveau pour la capacité d'orientation ? Comment fonctionne le GPS de notre cerveau ? Est-il similaire aux GPS technologiques ? Peut-on développer notre GPS cérébral ou est-ce une fatalité d'être mauvais en orientation ? Production, animation, réalisation et illustration : Anaïs RouxInstagram : https://www.instagram.com/neurosapiens.podcast/neurosapiens.podcast@gmail.comMusique d'intro KEEP ON GOINGMusique proposée par La Musique LibreJoakim Karud - Keep On Going : https://youtu.be/lOfg0jRqaA8Joakim Karud : https://soundcloud.com/joakimkarudSOURCESMünzer, S., Zimmer, H. D., Schwalm, M., Baus, J., & Aslan, I. (2006). Computer-assisted navigation and the acquisition of route and survey knowledge. Journal of Environmental Psychology, 26(4), 300–308. https://doi.org/10.1016/j.jenvp.2006.08.001Münzer S, Zimmer HD, Baus J. Navigation assistance: a trade-off between wayfinding support and configural learning support. J Exp Psychol Appl. 2012 Mar;18(1):18-37. doi: 10.1037/a0026553. Epub 2011 Dec 5. PMID: 22141461.Moser MB, Rowland DC, Moser EI. Place cells, grid cells, and memory. Cold Spring Harb Perspect Biol. 2015 Feb 2;7(2):a021808. doi: 10.1101/cshperspect.a021808. PMID: 25646382; PMCID: PMC4315928.Moser EI, Roudi Y, Witter MP, Kentros C, Bonhoeffer T, Moser MB. Grid cells and cortical representation. Nat Rev Neurosci. 2014 Jul;15(7):466-81. doi: 10.1038/nrn3766. Epub 2014 Jun 11. PMID: 24917300.Kropff, E., Carmichael, J., Moser, MB. et al. Speed cells in the medial entorhinal cortex. Nature 523, 419–424 (2015). https://doi.org/10.1038/nature14622Woollett, K. Talent in the taxi: A model system for exploring expertise. June 2009. Philosophical Transactions of The Royal Society B Biological Sciences 364(1522):1407-16. DOI:10.1098/rstb.2008.0288Spiers HJ, Maguire EA. A navigational guidance system in the human brain. Hippocampus. 2007;17(8):618-26. doi: 10.1002/hipo.20298. PMID: 17492693; PMCID: PMC2570439.Javadi, AH., Emo, B., Howard, L. et al. Hippocampal and prefrontal processing of network topology to simulate the future. Nat Commun 8, 14652 (2017). https://doi.org/10.1038/ncomms14652https://lejournal.cnrs.fr/articles/les-dessous-du-gps-cerebral Voir Acast.com/privacy pour les informations sur la vie privée et l'opt-out. Become a member at https://plus.acast.com/s/neurosapiens.

References Dr. Guerra's Lecture Notes Journal of the American College of Nutrition. 2019. 38:8, 693-702. Curr Diabetes Rev. 2020;16(8):797-806 --- Send in a voice message: https://anchor.fm/dr-daniel-j-guerra/message Support this podcast: https://anchor.fm/dr-daniel-j-guerra/support