Podcasts about inhibitory

Black cumin, also known as black seed oil, is an ancient remedy that has a multitude of surprising benefits! I was very impressed to find it improves fungal overgrowth, thyroid health, cholesterol and more. I'll dive into 10 health benefits of black cumin plus offer my recommended protocols.   Watch more videos like this

Jay McClelland is a pioneer in the field of artificial intelligence and is a cognitive psychologist and professor at Stanford University in the psychology, linguistics, and computer science departments. Together with David Rumelhart, Jay published the two volume work Parallel Distributed Processing, which has led to the flourishing of the connectionist approach to understanding cognition. In this conversation, Jay gives us a crash course in how neurons and biological brains work. This sets the stage for how psychologists such as Jay, David Rumelhart, and Geoffrey Hinton historically approached the development of models of cognition and ultimately artificial intelligence. We also discuss alternative approaches to neural computation such as symbolic and neuroscientific ones. Patreon (bonus materials + video chat): https://www.patreon.com/timothynguyen Part I. Introduction 00:00 : Preview 01:10 : Cognitive psychology 07:14 : Interdisciplinary work and Jay's academic journey 12:39 : Context affects perception 13:05 : Chomsky and psycholinguists 8:03 : Technical outline Part II. The Brain 00:20:20 : Structure of neurons 00:25:26 : Action potentials 00:27:00 : Synaptic processes and neuron firing 00:29:18 : Inhibitory neurons 00:33:10 : Feedforward neural networks 00:34:57 : Visual system 00:39:46 : Various parts of the visual cortex 00:45:31 : Columnar organization in the cortex 00:47:04 : Colocation in artificial vs biological networks 00:53:03 : Sensory systems and brain maps Part III. Approaches to AI, PDP, and Learning Rules 01:12:35 : Chomsky, symbolic rules, universal grammar 01:28:28 : Neuroscience, Francis Crick, vision vs language 01:32:36 : Neuroscience = bottom up 01:37:20 : Jay's path to AI 01:43:51 : James Anderson 01:44:51 : Geoff Hinton 01:54:25 : Parallel Distributed Processing (PDP) 02:03:40 : McClelland & Rumelhart's reading model 02:31:25 : Theories of learning 02:35:52 : Hebbian learning 02:43:23 : Rumelhart's Delta rule 02:44:45 : Gradient descent 02:47:04 : Backpropagation 02:54:52 : Outro: Retrospective and looking ahead Image credits: http://timothynguyen.org/image-credits/ Further reading: Rumelhart, McClelland. Parallel Distributed Processing. McClelland, J. L. (2013). Integrating probabilistic models of perception and interactive neural networks: A historical and tutorial review   Twitter: @iamtimnguyen   Webpage: http://www.timothynguyen.org

In this episode I describe inhibitory indirect response PK-PD models. I describe how they work, how to set up the dataset for NONMEM, and how to code the model in NONMEM. This is the third of 4 episodes on different PK-PD models. Links discussed in the show: Indirect response PK-PD model equations Example NONMEM code for inhibitory indirect response PK-PD model You can connect with me on LinkedIn and send me a message Send me a message Sign up for my newsletter Copyright Teuscher Solutions LLC All Rights Reserved

GUEST OVERVIEW - Professor Bruce Hood is a specialist in the Science of Happiness; Cognitive development from a neuroscience perspective. Inhibitory control of thoughts and actions. Spatial representation and action. Naïve theories. The origin of adult magical reasoning from children's natural intuitions.

In this episode, we explore the intricacies of neuronal communication, delving into how neurons transmit signals through synaptic connections using neurotransmitters like glutamate and GABA. We also examine the effects of neurotoxins, such as heavy metals and environmental pollutants, on these critical synaptic pathways, leading to cognitive and neurological impairments. Lastly, we discuss neuroprotective strategies to mitigate neurotoxin exposure and promote optimal brain health. Topics: 1. Overview of Brain Cell Anatomy - Types of brain cells: neurons and glial cells. - Structure of neurons: - Soma (cell body): contains nucleus and organelles. - Dendrites: receive signals from other neurons. - Axon: transmits electrical impulses away from the soma. - Synaptic terminals: form synapses with target cells. 2. Neuronal Communication - Synapse structure: - Presynaptic terminal. - Synaptic cleft. - Postsynaptic membrane. - Neurotransmitters: - Role in neuronal communication. - Excitatory neurotransmitters (e.g., glutamate). - Inhibitory neurotransmitters (e.g., GABA). 3. Summary of Neuronal Communication - Recap of excitatory and inhibitory neurotransmitters. - Importance of maintaining proper neuronal communication. 4. Neurotoxins and Their Effects - Types of neurotoxins: - Heavy metals (e.g., lead, mercury, arsenic, cadmium, aluminum). - Chemical neurotoxins (e.g., organophosphates, solvents). - Biological toxins (e.g., mycotoxins). - Environmental pollutants (e.g., PCBs, dioxins). - Mechanisms of neurotoxin damage: - Disruption of neurotransmitter release. - Impairment of receptor function. - Interference with ion channel operation. 5. Example: Mercury's Impact on Cognitive Function - Pathway of mercury exposure and accumulation in the brain. - Disruption of calcium homeostasis and synaptic transmission. - Resulting cognitive impairments. 6. Strategies to Reduce Neurotoxin Exposure - Nutrition: - Opting for organic produce. - Washing produce properly. - Avoiding MSG and aspartame. - Limiting aluminum exposure (baking powder). - Evaluating cookware. - Avoiding farmed salmon. - Water and air quality: - Using water filtration to remove fluoride. - Choosing fluoride-free toothpaste. - Improving air quality and mold remediation. - Using air-purifying plants (e.g., aloe vera, English ivy). - Reducing exposure to places with highly-concentrated neurotoxic chemicals (e.g., nail salons). Thank you to our episode sponsor: ⁠⁠⁠Tremetes, LLC⁠ Use code CHLOE15 to get 15% off ⁠Tremetes' Turkey Tail⁠ Thanks for tuning in! Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Follow Chloe on TikTok @chloe_c_porter Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to purchase products, subscribe to our mailing list, and more! --- Support this podcast: https://podcasters.spotify.com/pod/show/chloe-porter6/support

Dr. Don and Professor Ben talk about the risks of eating baby carrots passed their expiration date. Dr. Don - not risky

GUEST 1 OVERVIEW: Professor Bruce Hood is a specialist in the Science of Happiness; Cognitive development from a neuroscience perspective. Inhibitory control of thoughts and actions. Spatial representation and action. Naïve theories. The origin of adult magical reasoning from children's natural intuitions. GUEST 2 OVERVIEW:  Dr Peter Spencer is a former Chartered Health Psychologist. Peter had written about the madness of crowds some 20 years ago in the 'Psychologist' magazine "which, in hindsight seemed to predict the mass formation psychosis of the last few years".

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.08.01.551579v1?rss=1 Authors: Sanghavi, S., Kar, K. Abstract: A spatially distributed population of neurons in the macaque inferior temporal (IT) cortex supports object recognition behavior, but the cell-type specificity of the population in forming behaviorally sufficient object decodes remain unclear. To address this, we recorded neural signals from the macaque IT cortex and compared the object identity information and the alignment of decoding strategies derived from putative inhibitory (Inh) and excitatory (Exc) neurons to the monkeys' behavior. We observed that while Inh neurons represented significant category information, decoding strategies based on Exc neural population activity outperformed those from Inh neurons in overall accuracy and their image-level match to the monkeys' behavioral reports. Interestingly, both Exc and Inh responses explained a fraction of unique variance of the monkeys' behavior, demonstrating a distinct role of the two cell types in generating object identity solutions for a downstream readout. We observed that current artificial neural network (ANN) models of primate ventral stream, designed with AI goals of performance optimization on image categorization, better predict Exc neurons (and its contribution to object recognition behavior) than Inh neurons. Beyond, the refinement of linking propositions between IT and object recognition behavior, our results guide the development of more biologically constrained brain models by offering novel cell-type specific neural benchmarks. 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/2023.07.11.548438v1?rss=1 Authors: Peerboom, C. N. E., Wijne, T. B., Wierenga, C. J. Abstract: During the first two postnatal weeks intraneuronal chloride concentrations in rodents gradually decrease, causing a shift from depolarizing to hyperpolarizing {gamma}-aminobutyric acid (GABA) responses. GABAergic depolarization in the immature brain is crucial for the formation and maturation of excitatory synapses, but when GABAergic signaling becomes inhibitory it no longer promotes synapse formation. Here we examined the role of chloride transporters in developing postnatal hippocampal neurons using furosemide, an inhibitor of the chloride importer NKCC1 and chloride exporter KCC2 with reported anticonvulsant effects. We treated organotypic hippocampal cultures made from 6 to 7-day old mice with 200 M furosemide from DIV1 to DIV8. Using perforated patch clamp recordings we observed that the GABA reversal potential was depolarized after acute furosemide application, but after a week of furosemide treatment the GABA reversal potential but was more hyperpolarized compared to control. Expression levels of the chloride cotransporters were unaffected after one week furosemide treatment. This suggests that furosemide inhibited KCC2 acutely, while prolonged treatment resulted in (additional) inhibition of NKCC1, but we cannot exclude changes in HCO3-. We assessed the effects of accelerating the GABA shift by furosemide treatment on inhibitory synapses onto CA1 pyramidal cells. Directly after cessation of furosemide treatment at DIV9, inhibitory synapses were not affected. However at DIV21, two weeks after ending the treatment, we found that the frequency of inhibitory currents was increased, and VGAT puncta density in stratum Radiatum was increased. In addition, cell capacitance of CA1 pyramidal neurons was reduced in furosemide-treated slices at DIV21 in an activity-dependent manner. Our results suggest that furosemide indirectly promotes inhibitory transmission, but the underlying mechanism remains unresolved. The furosemide-induced increase in inhibitory transmission might constitute an additional mechanism via which furosemide reduces seizure susceptibility in the epileptic brain. 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/2023.07.05.547662v1?rss=1 Authors: Zhao, X., Zhang, Y. E., Yang, L., Yang, Y. Abstract: The mammalian neocortex receives extensive cholinergic projections from the basal forebrain. Although it has been shown that acetylcholine (Ach) participates in learning-associated cortical plasticity, it's not clear whether Ach can directly modulate structural changes of cortical synapses. Using in vivo two-photon microscopy, we show that optogenetic and chemogenetic stimulation of cholinergic neurons in mouse basal forebrain leads to an increase in spine formation on apical dendrites of layer (L) 5 pyramidal neurons in auditory cortex and posterior parietal cortex, and these newly formed spines follow similar spatial rules as the spontaneously formed new spines. Selective blockage of Ach receptors (AchRs) revealed that nicotinic AchRs, but not muscarinic AchRs, are involved in the stimulation-triggered spine formation. Furthermore, {gamma}-Aminobutyric acid (GABA) transmission is required in this process, indicating that acetylcholine acts through GABAergic connections in promoting spine formation. Together, our findings demonstrate that acetylcholine can induce spine formation in both sensory and higher-order cortices, via activating nicotinic AchRs through GABAergic local circuitry. Our work established a direct link between Ach release and cortical spine formation in vivo, and shed light on synaptic mechanisms underlying Ach-associated cortical remapping and learning-induced plasticity. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.01.547328v1?rss=1 Authors: Wietek, J., Nozownik, A., Pulin, M., Saraf-Sinik, I., Matosevich, N., Malan, D., Brown, B. J., Dine, J., Levy, R., Litvin, A., Regev, N., Subramaniam, S., Bitton, E., Benjamin, A., Copits, B. A., Sasse, P., Rost, B. R., Schmitz, D., Soba, P., Nir, Y., Wiegert, J. S., Yizhar, O. Abstract: Information is transmitted between brain regions through the release of neurotransmitters from long-range projecting axons. Understanding how the activity of such long-range connections contributes to behavior requires efficient methods for reversibly manipulating their function. Chemogenetic and optogenetic tools, acting through endogenous G-protein coupled receptor (GPCRs) pathways, can be used to modulate synaptic transmission, but existing tools are limited in sensitivity, spatiotemporal precision, or spectral multiplexing capabilities. Here we systematically evaluated multiple bistable opsins for optogenetic applications and found that the Platynereis dumerilii ciliary opsin (PdCO) is an efficient, versatile, light-activated bistable GPCR that can suppress synaptic transmission in mammalian neurons with high temporal precision in-vivo. PdCO has superior biophysical properties that enable spectral multiplexing with other optogenetic actuators and reporters. We demonstrate that PdCO can be used to conduct reversible loss-of-function experiments in long-range projections of behaving animals, thereby enabling detailed synapse-specific functional circuit mapping. 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/2023.06.28.546829v1?rss=1 Authors: Rayi, P. R., Lev, S. M., Binshtok, A. M. Abstract: The excitatory and inhibitory interneurons of superficial laminae I-II of the spinal dorsal horn (SDH) receive and process pain-related information from the primary afferents and transmit it to the brain via the projection neurons. Thus, the interaction between excitatory and inhibitory SDH interneurons is crucial in determining the output from the spinal cord network. Disruption of this interaction in pathological conditions leads to increased SDH output to the higher brain centers, which could underlie pathological pain. Here, we examined whether the changes in the intrinsic SDH connectivity also occur with age, possibly underlying age-related increase in pain sensitivity. Using Vgat;tdTomato transgenic mouse line, we compared the spontaneous inhibitory postsynaptic currents (sIPSCs) in inhibitory tdTomato+ and excitatory tdTomato- interneurons between adult (3-5 m.o.) and aged (12-13 m.o.) mice. We demonstrate that in adult mice, the amplitude and frequency of the sIPSCs in the excitatory interneurons were significantly higher than in inhibitory interneurons. These differences were annulled in aged mice. Further, we show that in aged mice, excitatory neurons receive less inhibition than in adult mice. This could lead to overall disinhibition of the SDH network, which might underlie increased pain perception among the aged population. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In this episode, I talk about how and why Exposure and Response Prevention works.  I discuss..  - an overview of Exposure and Response Prevention (ERP) - the Habituation model - the Inhibitory Learning model - enhancing the effectiveness of ERP - and so much more  Head to my website at www.jennaoverbaughlpc.com to sign up for my free e-mail newsletter, grab your free "Imagine Your Recovered Life" PDF, and download your free “5 Must Know Strategies for Managing Anxiety and Intrusive Thoughts” video + access expertly crafted masterclasses just for you.  Course and more coming soon! Remember: this podcast is for informational purposes only and may not be the best fit for you and your personal situation. It shall not be construed as mental health or medical advice. The information and education provided here is not intended or implied to supplement or replace professional advice of your own professional mental health or medical treatment, advice, and/or diagnosis. Always check with your own physician or medical or mental health professional before trying or implementing any information read here. Jenna Overbaugh, LPC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.06.26.546410v1?rss=1 Authors: Neyama, H., Wu, Y., Nakaya, Y., Kato, S., Shimizu, T., Tahara, T., Shigeta, M., Inoue, M., Miyamichi, K., Matsushita, N., Mashimo, T., Miyasaka, Y., Watanabe, Y., Kobayashi, M., Kobayashi, K., Cui, Y. Abstract: Placebo analgesia is caused by inactive treatment, implicating endogenous brain function involvement. However, the underlying neurobiological mechanisms remain unclear. We found that -opioid signals in the medial prefrontal cortex (mPFC) activate the descending pain inhibitory system to initiate placebo analgesia in neuropathic pain rats. Chemogenetic manipulation demonstrated that specific activation of -opioid receptor-positive (MOR+) neurons in the mPFC or suppression of the mPFC-ventrolateral periaqueductal gray (vlPAG) circuit inhibited placebo analgesia in rats. MOR+ neurons in the mPFC are monosynaptically connected and directly inhibit L5 pyramidal neurons that project to the vlPAG via GABAA receptors. Thus, intrinsic opioid signaling in the mPFC disinhibits excitatory outflow to the vlPAG by suppressing MOR+ neurons, leading to descending pain inhibitory system activation that initiates placebo analgesia. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In this Papers Podcast, Dr. Tone Hermansen discusses her JCPP Advances paper ‘Child internalizing and externalizing behaviors: Interplay between maternal depressive symptoms and child inhibitory control'.

Executive function refers to a set of cognitive processes that enables you to plan, organize, initiate, monitor, and adapt your behavior in order to achieve goals. It involves the higher-order control and regulation of other cognitive processes, allowing individuals to manage and coordinate their thoughts, actions, and emotions effectively. Executive function encompasses a range of mental abilities and skills that are essential for daily functioning. These include: Planning and organization: The ability to create a structured approach for achieving a goal, breaking it down into manageable steps, and determining the order in which tasks should be completed. Working memory: The capacity to temporarily hold and manipulate information in mind, allowing individuals to keep relevant information active while performing tasks or solving problems. Attentional control: The ability to focus and sustain attention on a specific task or stimuli, while filtering out distractions and irrelevant information. Cognitive flexibility: The capacity to adapt thinking and behavior in response to changing situations or demands. It involves shifting between different tasks or strategies and adjusting to new rules or perspectives. Inhibitory control: The ability to inhibit or suppress impulsive or automatic responses, allowing individuals to pause, think, and choose more appropriate behaviors or actions. Decision-making: The process of evaluating different options, weighing pros and cons, and selecting the most appropriate course of action based on desired goals and outcomes. Emotional regulation: The skill of managing and regulating emotions in order to appropriately respond to and cope with various situations. It involves recognizing and understanding one's own emotions and those of others, as well as effectively controlling emotional reactions. Executive function skills are crucial for academic and professional success, as well as for managing daily life tasks. They enable you to plan and prioritize tasks, stay organized, stay focused on goals, solve problems, make informed decisions, and regulate their behavior and emotions. While executive function abilities naturally develop throughout childhood and adolescence, they continue to mature into early adulthood. However, executive function can be impaired or disrupted due to various factors, such as brain injury, neurodevelopmental disorders (e.g., ADHD), neurodegenerative diseases (e.g., Alzheimer's), or mental health conditions. Understanding executive function is important as it allows you to recognize and address challenges you may face in areas such as time management, organization, impulse control, and decision-making. By improving executive function skills, individuals can enhance their overall cognitive abilities, productivity, and adaptability in various aspects of life. Let's chat about it. Become A Patreon www.patreon.com/thepositivityxperience For More Info: www.thepositivityxperience.com

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.05.04.539450v1?rss=1 Authors: Niraula, S., Yan, S. S., Subramanian, J. Abstract: Alzheimer's disease is associated with altered neuronal activity, presumably due to impairments in homeostatic synaptic plasticity. Neuronal hyper and hypoactivity are also observed in mouse models of amyloid pathology. Using multicolor two-photon microscopy, we test how amyloid pathology alters the structural dynamics of excitatory and inhibitory synapses and their homeostatic adaptation to altered experience-evoked activity in vivo in a mouse model. The baseline dynamics of mature excitatory synapses and their adaptation to visual deprivation are not altered in amyloidosis. Likewise, the baseline dynamics of inhibitory synapses are not affected. In contrast, despite unaltered neuronal activity patterns, amyloid pathology leads to a selective disruption of homeostatic structural disinhibition on the dendritic shaft. We show that excitatory and inhibitory synapse loss is locally clustered under the nonpathological state, but amyloid pathology disrupts it, indicating impaired communication of changes in excitability to inhibitory synapses. 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/2023.05.01.538911v1?rss=1 Authors: Niklaus, S., Glasauer, S. M. K., Kovermann, P., Farshori, K. F., Cadetti, L., Fruh, S., Rieser, N. N., Gesemann, M., Fahkle, C., Neuhauss, S. C. 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/2023.04.25.538236v1?rss=1 Authors: Bergoin, R., Torcini, A., Deco, G., Quoy, M., Zamora-Lopez, G. Abstract: Brain circuits display modular architecture at different scales of organization. Such neural assemblies are typically associated to functional specialization but the mechanisms leading to their emergence and consolidation still remain elusive. In this paper we investigate the role of inhibition in structuring new neural assemblies driven by the entrainment to various inputs. In particular, we focus on the role of partially synchronized dynamics for the creation and maintenance of structural modules in neural circuits by considering a network of excitatory and inhibitory theta-neurons with plastic Hebbian synapses. The learning process consists of an entrainment to temporally alternating stimuli that are applied to separate regions of the network. This entrainment leads to the emergence of modular structures. Contrary to common practice in artificial neural networks - where the acquired weights are typically frozen after the learning session - we allow for synaptic adaptation even after the learning phase. We find that the presence of inhibitory neurons in the network is crucial for the emergence and the post-learning consolidation of the modular structures. Indeed networks made of purely excitatory neurons or of neurons not respecting Dale's principle are unable to form or maintain the modular architecture induced by the entrained stimuli. We also demonstrate that the number of inhibitory neurons in the network is directly related to the maximal number of neural assemblies that can be consolidated, supporting the idea that inhibition has a direct impact on the memory capacity of the neural network. 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/2023.04.10.536138v1?rss=1 Authors: Broggini, A. C., Onorato, I., Tzanou, A., Sotomayor, B., Uran, C., Vinck, M. Abstract: Cortical information processing is thought to be facilitated by the resonant properties of individual neurons and neuronal networks, which selectively amplify inputs at specific frequencies. We used optogenetics to test how different input frequencies are encoded by excitatory cells and parvalbumin-expressing (PV) interneurons in mouse V1. Spike phase-locking and power increased with frequency, reaching a broad peak around 80-100Hz. This effect was observed only for Chronos, a fast-kinetic opsin, but not for Channelrhodopsin-2. Surprisingly, neurons did not exhibit narrow-band resonance in specific frequency-ranges, and showed reliably phase-locking up to 140Hz. Strong phase-locking at high frequencies reflected non-linear input/output transformations, with neurons firing only in a narrow part of the cycle. By contrast, low-frequency inputs were encoded in a more continuous manner. Correspondingly, spectral coherence and firing rates showed little dependence on frequency and did not reflect transferred power. To investigate whether strong phase-locking facilitated the reliable encoding of inputs, we analyzed various spike-train distances and Fano factor. Interestingly, responses to lower rather than higher frequencies had more globally reliable spike-counts and timing structure. These findings have various practical implications for understanding the effects of optogenetic stimulation and choice of opsin. Furthermore, they show both PV and excitatory neurons respond with more local precision, i.e. phase-locking, to high-frequency inputs, but have more globally reliable responses to low-frequency inputs, suggesting differential coding regimes for these frequencies. 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/2023.04.07.536092v1?rss=1 Authors: Gehr, C., Sibille, J., Kremkow, J. Abstract: The superior colliculus (SC) is a midbrain structure that contains one of the highest densities of inhibitory neurons in the brain and, together with the thalamocortical visual system, it plays a key role in visually guided behaviors. The SC receives direct inputs from retinal ganglion cells (RGCs) but whether excitatory and inhibitory SC neurons differentially integrate retinal activity in vivo is still largely unknown. We recently established an extracellular recording approach using high-density electrodes to measure the activity of RGCs simultaneously with their postsynaptic SC targets in vivo, that allows addressing how SC neurons integrate RGC activity. Here, we employ this method to study the functional properties and dynamics that govern retinocollicular signaling in a cell-type specific manner by identifying GABAergic SC neurons using optotagging in anesthetized VGAT-ChR2 mice. We measured 305 monosynaptically connected RGC-SC pairs, out of which approximately one third of retinal afferents connect onto inhibitory SC neurons. We show that both excitatory and inhibitory SC neurons receive comparable strong RGC inputs, with functionally similar RGC-SC pairs showing stronger connections. Our results demonstrate that similar wiring rules apply for RGCs innervation of both excitatory and inhibitory SC neurons, which is unlike the cell-type specific connectivity in the thalamocortical system. Contrasting the similar RGC-SC connection strength, we observed that RGC activity contributed more to the activity of postsynaptic excitatory SC neurons than to the activity of postsynaptic inhibitory SC neurons. This implies that the excitatory SC neurons are more specifically coupled to RGC afferent inputs, while inhibitory SC neurons may integrate additional inputs from other sources. Taken together, our study deepens the understanding of cell-type specific retinocollicular functional connectivity and emphasizes that the two major brain areas for visual processing, the visual cortex and the superior colliculus, differently integrate sensory afferent inputs. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Dr Jonathan Abramowitz is a clinical psychologist, author, and Professor for the Department of Psychology and Neuroscience at the University of North Carolina in America. With over 25 years of experience, Jon is recognised internationally as a leading authority on the treatment and study of OCD and is dedicated to researching and publishing his findings on OCD treatment and passing on his knowledge to the next generation of clinical psychology students.  In today's episode, Jon explains how to integrate the inhibitory learning model into clinical practice and the importance of maintaining consistency in that process. He then shares his difficulty in knowing that the first edition of his book, "Getting Over OCD: A 10-Step Workbook for Taking Back Your Life", is still in circulation. This episode is part two of our two-part conversation with Dr Jonathan Abramowitz. Check out our last episode, where Jon introduces us to his insights on the inhibitory learning model.   Resources and links: Dr Jonathan Abramowitz website   Connect: https://www.melbournewellbeinggroup.com.au/ http://www.drcelingelgec.com.au/ This show is produced in collaboration with Wavelength Creative. Visit wavelengthcreative.com for more information.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.03.535448v1?rss=1 Authors: Irala, D., Wang, S., Sakers, K., Nagendren, L., Ulloa-Severino, F. P., Bindu, D. S., Eroglu, C. Abstract: Astrocytes strongly promote the formation and maturation of synapses by secreted proteins. To date, several astrocyte-secreted synaptogenic proteins controlling different stages of excitatory synapse development have been identified. However, the identities of astrocytic signals that induce inhibitory synapse formation remain elusive. Here, through a combination of in vitro and in vivo experiments, we identified Neurocan as an astrocyte-secreted inhibitory synaptogenic protein. Neurocan is a chondroitin sulfate proteoglycan that is best known as a protein localized to the perineuronal nets. However, Neurocan is cleaved into two after secretion from astrocytes. We found that the resulting N- and C- terminal fragments have distinct localizations in the extracellular matrix. While the N-terminal fragment remains associated with perineuronal nets, the Neurocan C-terminal fragment localizes to synapses and specifically controls cortical inhibitory synapse formation and function. Neurocan knockout mice lacking the whole protein or only its C-terminal synaptogenic region have reduced inhibitory synapse numbers and function. Through super-resolution microscopy and in vivo proximity labeling by secreted TurboID, we discovered that the synaptogenic domain of Neurocan localizes to somatostatin-positive inhibitory synapses and strongly regulates their formation. Together, our results unveil a mechanism through which astrocytes control circuit-specific inhibitory synapse development in the mammalian brain. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In this episode of the Smarter Not Harder Podcast, our guest Dr. Andrew Gallimore joins our host Dr. Ted Achachoso to give 1 cent solutions to the following $64,000 questions:   Does dimethyltryptamine make the brain construct a different reality or does it make the brain perceive a different reality based on the information that it was receiving?  How do molecules such as LSD, DMT, psilocybin, and mescaline switch one's reality from one channel to another Why is the fly agaric psychedelic?     Dr. Andrew Gallimore is a British neurobiologist, chemist, pharmacologist and writer based in Tokyo, Japan. He has been interested in the relationship between psychedelic drugs, the brain, consciousness, and the structure of reality. He has written a couple of books that he illustrated and self-published. His works are Alien Information Theory: Psychedelic Drug Technologies, and the Cosmic Game (2019), and Reality Switch Technologies: Psychedelics as Tools for the Discovery and Exploration of New Worlds (2022).     What we discuss:   [00:00] Dr. Andrew Gallimore discusses his self-published book on psychedelic drug technologies and the structure of reality [09:12] DMT and Conway's Game of Life illustrate the emergence of complexity from simple rules [25:29] DMT experience reveals highly intelligent, hyper-dimensional space beyond our reality [34:06] DMT allows the brain to construct an alternate reality without affecting critical parts. [49:36] Salvanorin inhibits the claustrum, which releases the cortex and creates novel emergent patterns of activity. [57:19] Salvia tears apart the fabric of reality while classic psychedelics allow the brain to reach new states [1:12:43] Different drugs affect perception and reality in different ways. [1:20:42] Inhibitory interneurons control excitation inhibition balance [1:36:11] Positive allosteric modulators can enhance receptor activity without the presence of an endogenous agonist. [00:15] Muscimol and its Psychedelic Properties   Find more from Smarter Not Harder: Website: https://troscriptions.com/blogs/podcast | https://homehope.org Instagram: @troscriptions | @homehopeorg   Find out more about Dr. Andrew Gallimore: Website: http://alieninsect.net/ Twitter: @alieninsect Instagram: @alieninsect YouTube: youtube.com/c/alieninsect  Books: Alien Information Theory: Psychedelic Drug Technologies and the Cosmic Game Reality Switch Technologies: Psychedelics as Tools for the Discovery and Exploration of New Worlds     Get 10% Off Your Purchase of Metabolomics Module by using PODCAST10 at https://www.homehope.org   Get 10% Off your Troscriptions purchase by using POD10 at https://www.troscriptions.com   Get daily content from the hosts of Smarter Not Harder by following @troscriptions on Instagram. 

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.24.534013v1?rss=1 Authors: McGill, M., Kremer, C., Stecyk, K., Clayton, K., Skerleva, D., Hancock, K., Kujawa, S. G., Polley, D. B. Abstract: Sound perception is closely linked to the spatiotemporal patterning of neural activity in the auditory cortex (ACtx). Inhibitory interneurons sculpt the patterns of excitatory ACtx pyramidal neuron activity, and thus play a central role in sculpting the perception of sound. Reduced inhibition from parvalbumin-expressing (PV) inhibitory interneurons and the associated increased gain of sound-evoked pyramidal neuron spike rates are well-established consequences of aging and sensorineural hearing loss. Here, we reasoned that changes in PV-mediated inhibition would directly impact the perception of loudness. We hypothesized that ACtx PV activity could function as a perceptual volume knob, where reduced or elevated PV activity would increase or decrease the perceived loudness of sound, respectively. To test these hypotheses, we developed a two-alternative forced-choice loudness classification task for head-fixed mice and demonstrated that noise-induced sensorineural hearing loss directly caused a ~10 dB loudness hyperacusis that begins hours after noise-induced sensorineural hearing loss and persists for at least several weeks. Conversely, sounds were perceived as ~10 dB softer during optogenetic activation of ACtx PV neurons without having any effect on the overall detectability of sound. These data suggest that ACtx PV neurons can bi-directionally control the perceived loudness of sound, presumably via the strength of their inhibition onto local pyramidal neurons. Further, these data identify cortical PV neurons as a target for hyperacusis therapies and demonstrate a direct link between acquired sensorineural hearing loss and loudness hyperacusis. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.22.533751v1?rss=1 Authors: Muellner, F. E., Roska, B. Abstract: Inhibitory interneurons in the dorsolateral geniculate nucleus (dLGN) are situated at the first central synapse of the image-forming visual pathway but little is known about their function. Given their anatomy, they are expected to be multiplexors, integrating many different retinal channels along their dendrites. Here, using targeted single-cell-initiated rabies tracing, we found that mouse dLGN interneurons exhibit a degree of retinal input specialization similar to thalamocortical neurons. Some are anatomically highly specialized, for example, towards direction-selective information. Two-photon calcium imaging performed in vivo revealed that interneurons are also functionally specialized. In mice lacking retinal horizontal direction selectivity, horizontal direction selectivity is reduced in interneurons, suggesting a causal link between input and functional specialization. Functional specialization is not only present at interneuron somata, but also extends into their dendrites. Altogether, each inhibitory interneuron globally encodes one visual feature originating mostly in the retina and is ideally suited to perform feature-selective inhibition. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.21.533603v1?rss=1 Authors: Hayashi, M., Gullo, M., Senturk, G., Di Costanzo, S., Nagasaki, S. C., Kageyama, R., Imayoshi, I., Goulding, M., Pfaff, S. L., Gatto, G. Abstract: Innate and goal-directed movements require a high-degree of trunk and appendicular muscle coordination to preserve body stability while ensuring the correct execution of the motor action. The spinal neural circuits underlying motor execution and postural stability are finely modulated by propriospinal, sensory and descending feedback, yet how distinct spinal neuron populations cooperate to control body stability and limb coordination remains unclear. Here, we identified a spinal microcircuit composed of V2 lineage-derived excitatory (V2a) and inhibitory (V2b) neurons that together coordinate ipsilateral body movements during locomotion. Inactivation of the entire V2 neuron lineage does not impair intralimb coordination but destabilizes body balance and ipsilateral limb coupling, causing mice to adopt a compensatory festinating gait and be unable to execute skilled locomotor tasks. Taken together our data suggest that during locomotion the excitatory V2a and inhibitory V2b neurons act antagonistically to control intralimb coordination, and synergistically to coordinate forelimb and hindlimb movements. Thus, we suggest a new circuit architecture, by which neurons with distinct neurotransmitter identities employ a dual-mode of operation, exerting either synergistic or opposing functions to control different facets of the same motor behavior. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.20.533583v1?rss=1 Authors: Song, S.-H., Augustine, G. J. Abstract: Synapsins cluster synaptic vesicles (SVs) to provide a reserve pool (RP) of SVs that maintains synaptic transmission during sustained activity. However, it is unknown how synapsins cluster SVs. Here we show that either liquid-liquid phase separation (LLPS) or tetramerization-dependent cross-linking can cluster SVs, depending upon whether a synapse is excitatory or inhibitory. Cell-free reconstitution revealed that both mechanisms can cluster SVs, with tetramerization bring more effective. At inhibitory synapses, perturbing synapsin-dependent LLPS impairs SV clustering and synchronization of GABA release, while perturbing synapsin tetramerization does not. At glutamatergic synapses, the opposite is true: synapsin tetramerization enhances clustering of glutamatergic SVs and mobilization of these SVs from the RP, while synapsin LLPS does not. Comparison of inhibitory and excitatory transmission during prolonged synaptic activity revealed that synapsin LLPS serves as a brake to limit GABA release, while synapsin tetramerization enables rapid mobilization of SVs from the RP to sustain glutamate release. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Dr Jonathan Abramowitz is a world-renowned clinical psychologist and a Professor in the Department of Psychology and Neuroscience at the University of North Carolina. Jon has over 25 years of experience working in the treatment of OCD and related disorders and has contributed to hundreds of scientific publications in that time. He also trains clinical psychology students and is the author of several books and book chapters.  In today's episode, Jon explains how he came to be involved with OCD treatment and research in the first place. He shares his insights on the evolution of the inhibitory learning model and details how it can be used to modify ERP and treat OCD. This episode is part one of our two-part conversation with Dr Jonathan Abramowitz. Keep an eye out for our next episode, where Jon delves deeper into how to integrate the inhibitory learning model into practice.   Resources and links: Dr Jonathan Abramowitz website   Connect: https://www.melbournewellbeinggroup.com.au/ http://www.drcelingelgec.com.au/ This show is produced in collaboration with Wavelength Creative. Visit wavelengthcreative.com for more information.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.16.532850v1?rss=1 Authors: Barron, J. J., Mroz, N. M., Taloma, S. E., Dahlgren, M. W., Ortiz-Carpena, J. F., Dorman, L. C., Vainchtein, I. D., Escoubas, C. C., Molofsky, A. B., Molofsky, A. V. Abstract: The innate immune system plays essential roles in brain synaptic development, and immune dysregulation is implicated in neurodevelopmental diseases. Here we show that a subset of innate lymphocytes (group 2 innate lymphoid cells, ILC2s) is required for cortical inhibitory synapse maturation and adult social behavior. ILC2s expanded in the developing meninges and produced a surge of their canonical cytokine Interleukin-13 (IL-13) between postnatal days 5-15. Loss of ILC2s decreased cortical inhibitory synapse numbers in the postnatal period where as ILC2 transplant was sufficient to increase inhibitory synapse numbers. Deletion of the IL-4/IL-13 receptor (Il4ra) from inhibitory neurons phenocopied the reduction inhibitory synapses. Both ILC2 deficient and neuronal Il4ra deficient animals had similar and selective impairments in adult social behavior. These data define a type 2 immune circuit in early life that shapes adult brain function. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.14.532493v1?rss=1 Authors: Cheng, Y.-T., Luna-Figueroa, E., Woo, J., Chen, H.-C., Lee, Z.-F., Harmanci, A. S., Deneen, B. Abstract: Communication between neurons and glia plays an important role in establishing and maintaining higher order brain function. Astrocytes are endowed with complex morphologies which places their peripheral processes in close proximity to neuronal synapses and directly contributes to their regulation of brain circuits. Recent studies have shown that excitatory neuronal activity promotes oligodendrocyte differentiation; whether inhibitory neurotransmission regulates astrocyte morphogenesis during development is unknown. Here we show that inhibitory neuron activity is necessary and sufficient for astrocyte morphogenesis. We found that input from inhibitory neurons functions through astrocytic GABABR and that its deletion in astrocytes results in a loss of morphological complexity across a host of brain regions and disruption of circuit function. Expression of GABABR in developing astrocytes is regulated in a region-specific manner by SOX9 or NFIA and deletion of these transcription factors results in region-specific defects in astrocyte morphogenesis, which is conferred by interactions with transcription factors exhibiting region-restricted patterns of expression. Together our studies identify input from inhibitory neurons and astrocytic GABABR as universal regulators of morphogenesis, while further revealing a combinatorial code of region-specific transcriptional dependencies for astrocyte development that is intertwined with activity-dependent processes. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.14.532664v1?rss=1 Authors: Ferguson, K. A., Salameh, J., Alba, C., Selwyn, H., Barnes, C., Lohani, S., Cardin, J. A. Abstract: Local cortical circuit function is regulated by diverse populations of GABAergic interneurons with distinct properties and extensive interconnectivity. Inhibitory-to-inhibitory interactions between interneuron populations may play key roles in shaping circuit operation according to behavioral context. A specialized population of GABAergic interneurons that co-express vasoactive intestinal peptide (VIP-INs) are activated during arousal and locomotion and synapse on other local interneurons and pyramidal neurons. Although modulation of VIP-IN activity by behavioral state has been extensively studied, their role in regulating information processing and selectivity is less well understood. Using a combination of cellular imaging, short- and long-term manipulation, and perceptual behavior, we examined the impact of VIP-INs on their synaptic target populations in the primary visual cortex of awake behaving mice. We find that loss of VIP-IN activity alters the behavioral state-dependent modulation of somatostatin-expressing interneurons (SST-INs) but not pyramidal neurons (PNs). In contrast, reduced VIP-IN activity disrupts visual feature selectivity for stimulus size in both populations. Inhibitory-to-inhibitory interactions thus directly shape the selectivity of GABAergic interneurons for sensory stimuli. Moreover, the impact of VIP-IN activity on perceptual behavior varies with visual context and is more acute for small than large visual cues. VIP-INs thus contribute to both state-dependent modulation of cortical circuit activity and sensory context-dependent perceptual performance. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.02.530499v1?rss=1 Authors: Barbour, A. J., Gourmaud, S., Li, X., Stewart, D. A., Irwin, D. J., Talos, D. M., Jensen, F. E. Abstract: Increasing evidence indicates a bidirectional relationship between epilepsy and Alzheimer's disease (AD) with 22% of AD patients additionally suffering from seizures, which may be a targetable component of disease progression. Since epileptogenesis is associated with changes in excitatory: inhibitory (E:I) balance, we examined postmortem AD brain tissue from patients with and without seizure history and five times familial AD (5XFAD) mice for changes in several markers of E:I balance, including the inhibitory GABAA receptor, the chloride cotransporters, sodium potassium chloride cotransporter 1 (NKCC1) and potassium chloride cotransporter 2 (KCC2), and the excitatory NMDA and AMPA type glutamate receptors. We hypothesized that seizure history in AD patients would be associated with greater E:I imbalances, and that such changes would also be observed in the 5XFAD mice following pentylenetetrazol (PTZ) kindling. We found that seizures in AD patients were associated with alterations in NKCC1 and KCC2 expression, indicative of depolarizing GABA, and exacerbated cognitive deficits. Seizures also significantly contributed to E:I imbalance in the 5XFAD mouse model, as similar changes in NKCC1 and KCC2 expression were found in PTZ treated 5XFAD mice, along with altered AMPA receptor protein expression indicative of calcium permeable-AMPA receptors. In addition, we found that chronic treatment with the mTOR inhibitor rapamycin at doses we have previously shown to attenuate seizure-induced {beta}-amyloid pathology and cognitive deficits in 5XFAD mice, can mitigate the dysregulation of markers of E:I balance in this model. These data suggest that mTOR activation plays a role in modifying the E:I imbalance and network hyperexcitability in AD and that the FDA-approved mTOR inhibitors such as rapamycin may have potential for therapy in AD patients with a seizure history. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.01.530698v1?rss=1 Authors: Zhao, L., Silva, A. B., Kurteff, G. L., Chang, E. F. Abstract: Natural speech is full of starts and stops. Here, we studied the neural mechanisms that underlie the inhibitory control of speech, specifically the ability to stop speaking on demand. We recorded direct cortical activity while participants made continuous speech production and were given a visual cue to stop speaking. Neural recordings revealed activity in the premotor frontal cortex associated with speech stopping. Cortical sites showing stop activity were largely distinct from sites involved in active speech production or, more specifically, encoding articulatory movements. Electrocortical stimulation mapping at many premotor sites with stop activity caused involuntary speech arrest, an immediate inability to speak or vocalize. Furthermore, many speech arrest sites did not co-localize with neural activity correlating with speech motor planning or execution, contrary to this long-assumed function in clinical brain mapping. Together, these results suggest a previously unknown premotor cortical network that underlies the inhibitory control of speech, which has significant implications for understanding the dynamics of normal and altered speech production, as well as clinical brain mapping. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.14.528229v1?rss=1 Authors: Wu, J., Quraishi, I. H., Zhang, Y., Bromwich, M., Kaczmarek, L. K. Abstract: KCNT1 encodes the sodium-activated potassium channel Slack (KCNT1, KNa1.1), an important mediator of neuronal membrane excitability. Gain-of-function (GOF) mutations in humans lead cortical network hyperexcitability and seizures, as well as very severe intellectual disability. Using a mouse model of Slack GOF-associated epilepsy, we found that both excitatory and inhibitory neurons of the cerebral cortex have increased Na+-dependent K+ (KNa) currents and voltage-dependent sodium (NaV) currents. The characteristics of the increased KNa currents were, however, different in the two cell types such that the intrinsic excitability of excitatory neurons was enhanced but that of inhibitory neurons was suppressed. We further showed that the expression of NaV channel subunits, particularly that of NaV1.6, is upregulated and that the length of the axon initial segment (AIS) and of axonal NaV immunostaining is increased in both neuron types. We found that the proximity of the AIS to the soma is shorter in excitatory neurons than in inhibitory neurons of the mutant animals, potentially contributing to the different effects on membrane excitability. Our study on the coordinate regulation of KNa currents and the expression of NaV channels may provide a new avenue for understanding and treating epilepsies and other neurological disorders. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.10.528013v1?rss=1 Authors: Boyle, K. A., Polgar, E., Gutierrez-Mecinas, M., Dickie, A. C., Cooper, A. H., Bell, A. M., Jumolea, E., Casas-Benito, A., Watanabe, M., Hughes, D. I., Weir, G., Riddell, J., Todd, A. J. Abstract: Somatosensory information is processed by a complex network of interneurons in the spinal dorsal horn. It has been reported that inhibitory interneurons that express neuropeptide Y (NPY), either permanently or during development, suppress mechanical itch, with no effect on pain. Here we investigate the role of interneurons that continue to express NPY (NPY-INs) in adulthood. We find that chemogenetic activation of NPY-INs reduces behaviours associated with acute pain and pruritogen evoked itch, whereas silencing them causes exaggerated itch responses that depend on cells expressing the gastrin-releasing peptide receptor. As predicted by our previous studies, silencing of another population of inhibitory interneurons (those expressing dynorphin) also increases itch, but to a lesser extent. Importantly, NPY IN activation also reduces behavioural signs of inflammatory and neuropathic pain. These results demonstrate that NPY-INs gate pain and itch transmission at the spinal level, and therefore represent a potential treatment target for pathological pain and itch. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.06.527263v1?rss=1 Authors: Emerson, J., Delgado, T., Girardi, P., Johnson, G. V. Abstract: AAstrocytes are the primary support cells of the central nervous system (CNS) that help maintain the energetic requirements and homeostatic environment of neurons. CNS injury causes astrocytes to take on reactive phenotypes with altered overall function that can range from supportive to harmful for recovering neurons. The characterization of reactive astrocyte populations is a rapidly developing field, and the underlying factors and signaling pathways governing which type of reactive phenotype that astrocytes take on is poorly understood. Our previous studies suggest that transglutaminase 2 (TG2) has an important role in determining the astrocytic response to injury. TG2 is upregulated in astrocytes across multiple injury models, and selectively deleting TG2 from astrocytes improves functional outcomes after CNS injury and causes widespread changes in gene regulation, which is associated with its nuclear localization. The underlying molecular mechanisms by which TG2 causes these functional changes are unknown, and its interactions in the nucleus of astrocytes has not yet been described. To begin to understand how TG2 impacts astrocytic function, we used a neuron-astrocyte co-culture paradigm to compare the effects of TG2-/- and wild type (WT) astrocytes on neurite outgrowth and synapse formation. We assayed neurons on both a growth-supportive substrate and an injury-simulating matrix comprised of inhibitory chondroitin sulfate proteoglycans (CSPGs). Compared to WT astrocytes, TG2-/- astrocytes supported neurite outgrowth to a significantly greater extent only on the CSPG matrix, while synapse formation assays showed mixed results depending on the pre- and post-synaptic markers analyzed. We hypothesize that TG2 regulates the supportive functions of astrocytes in injury conditions by modulating the expression of a wide range of genes through interactions with transcription factors and transcription complexes. Based on results of a previous yeast two-hybrid screen for TG2 interactors, we further investigated the interaction of TG2 with Zbtb7a, a ubiquitously expressed transcription factor. Co-immunoprecipitation and colocalization analyses confirmed the interaction of TG2 and Zbtb7a in the nucleus of astrocytes. Genetic overexpression or knockdown of Zbtb7a levels in TG2-/- and WT astrocytes revealed that Zbtb7a robustly influenced astrocytic morphology and the ability of astrocytes to support neuronal outgrowth, which was significantly modulated by the presence of TG2. These findings support our hypothesis that astrocytic TG2 acts as a transcriptional regulator to influence astrocytic function, with greater influence under injury conditions that increase its expression, and Zbtb7a likely contributes to the overall effects observed with astrocytic TG2 deletion. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

In the second episode of Season 3, Naomi sits down with Dr. Amy Egbert of the University of Connecticut to talk about her research on eating disorders and disordered eating patterns among youth from underrepresented and marginalized backgrounds. Importantly, Dr. Egbert discusses her investigation into how race and ethnicity have been reported in eating disorder studies over the last 20 years, including the trends and long-term implications. As another area of research interest, Naomi and Amy also touch on how food marketing plays a role in the development of disordered eating and eating disorders. As a new faculty at UConn, Naomi and Amy close up the episode chatting about her goals for her brand new lab!Papers Referenced in the Episode:1) Egbert et al., 2022: Reporting racial and ethnic diversity in eating disorder research over the past 20 years. International Journal of Eating Disorders / Vol. 55, Issue 4.2) Egbert et al., 2022: Delicious and difficult to resist?: Inhibitory control differs in young women after exposure to food and non-food commercials. Appetite.  June 1; 173Follow/Contact Picture Blurrfect:Twitter: @BlurrfectInstagram: @picture_blurrfectE-mail: naomi.charalambakis90@gmail.com 

How Does Exposure Work For Anxiety? Habituation vs Inhibitory Learning We know about exposure. Going toward the thing we fear rather than trying to avoid it, escape from it, or engineer life so that it is never “triggered”. We know that exposure is en effective tool when it comes to anxiety disorders. But how does it actually work? Why does it sometimes only work halfway? Why does it sometimes not last? What is habituation? What is inhibitory learning? Let's get geeky with it this week! For full show notes on this episode: https://theanxioustruth.com/226 --- My books, social, and other links: https://theanxioustruth.com/links Support The Anxious Truth: https://theanxioustruth.com/support Music Credit: AfterGlow by Ben Drake (with permission) https://bendrakemusic.com

In this episode, Darius and Erica share some personal life hacks, tools, and technology to develop inhibitory control skills. - how inhibitory control works - personal executive function hacks - Time blocking - Calendars - Reminders - Managing your environment - physical - visual - desk position - Lighting - Clothing - uniform - shoes - glasses - Sound quality - Creating a focused routine Technology - Split screens - Thesaurus - TickTick - Asana - Google Calendar - Google Keep - FM Systems - Airpods and headphones (noise cancelling) - Zoom Links - Eisenhower's Urgent/Important Principle: https://tinyurl.com/yc5r2hs6 - Google Keep: https://keep.google.com/ - Google Calendar: https://calendar.google.com/ - Asana: https://app.asana.com/ - Zoom: https://zoom.us/ - MindMapping - BulletMap Academy: https://bulletmapacademy.com/ - Good Sensory Learning: https://goodsensorylearning.com/ - Access to Work Advice: Contact Darius @ www.dyslexiawork.com - Learning Specialist Courses: https://www.learningspecialistcourses.com/ Brought to you by - www.goodsensorylearning.com - www.learningspecialistcourses.com - www.bulletmapacademy.com

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Are you good at doing things “right,” following the rules, and controlling your emotions? Maybe a little too good? Do people in your life sometimes have a hard time believing how much you're struggling with your mental health because you seem so “high functioning?” If so, you might have an Overcontrolled style of coping. This is a temperamentally based trait that means you are highly detail-focused, attuned to threat, and high in something called inhibitory control. Inhibitory control is the ability to inhibit one's impulses and behaviors. Many people who have an Overcontrolled style of coping look like they have it all together on the outside, but they don't feel like they do, and their suffering often goes unnoticed. Focusing too much on doing everything “right” can lead to rigidity, perfectionism, and loneliness, making it hard to connect with others and enjoy life. My guest on today's episode is Larry Dahmer – a psychological associate at Health Sciences North in Sudbury, Ontario CA who specializes in a new treatment modality for those who struggle with overcontrolled coping styles called Radically Open Dialectical Behavioral Therapy (RO-DBT.) Topics covered in this episode: ■ What is Radically Open Dialectical Behavioral Therapy (RO-DBT)?■ How is RO-DBT different from standard DBT?■ Understanding the problem of emotional overcontrol■ The importance of self-inquiry in RO-DBT■ How emotional overcontrol is praised and encouraged in Western society■ How we can “welcome hopelessness, despair and anxiety as teachers”■ Who might be a good fit for RO-DBT?■ Life-changing stories of transformation that Larry has witnessed in his RO-DBT clients Learn more about RO-DBT at https://www.radicallyopen.net/ See acast.com/privacy for privacy and opt-out information. Become a member at https://plus.acast.com/s/back-from-the-borderline.

OCD approaches are constantly evolving and changing. This is in part due to the wonderful, ongoing research around OCD.In recent years we've seen a growing number of OCD therapists incorporate ACT, Acceptance and Commitment Therapy, into OCD therapy. We've also seen more clinicians embrace the Inhibitory Learning Model approach and have seen practitioners adapt ERP (Exposure with Response Prevention) to reflect these changes.So what does this all mean?In this week's AT Parenting Survival Podcast I'll give you the short version of how this might impact how you help your child with OCD.Other Resources on the Inhibitory Learning Model:IOCDF: The Inhibitory Learning Approach to Exposure and Response PreventionYoutube videoIOCDF Research Roundtable: Habituation Therapy, Inhibitory Learning Model, and ACTThis podcast episode is sponsored by NOCD. NOCD provides online OCD therapy in the US, UK, Australia and Canada. To schedule your free 15 minute consultation to see if NOCD is a right fit for you and your child, go tohttps://go.treatmyocd.com/at_parentingThis podcast is for informational purposes only and should not be used to replace the guidance of a qualified professional.To join the AT Parenting Community go to: www.ATparentingcommunity.comVisit my website at www.ATparentingSurvival.comSign up for my weekly email newsletter:https://pages.convertkit.com/740ba8cd83/92109b7172 See acast.com/privacy for privacy and opt-out information.

Here's an intro to GABA and Serotonin deficiency and a short Brain Quiz to help tell the two apart. Welcome to your Brain! GABA and Serotonin are our two main inhibitory neurotransmitters. Inhibitory sounds like a bad thing, but we need balance between excitatory and inhibitory aspects in all functions in the body. Just as there's light and dark, and fast and slow, we need both in balance. Why do we need Inhibitory and Excitatory Neurotransmitters in balance? Read More

Inhibitory Control - Inhibitory control, also known as response inhibition, is an executive function – that permits an individual to inhibit their impulses and habitual behavioral responses in order to select a more appropriate behavior that is consistent with completing a task or goal. Ability to block distractions - Editing your moment - MUTE Links for reference of the topic - Jill Bolte Taylor: https://www.drjilltaylor.com/ - 90 Second Rule: https://youtu.be/vxARXvljKBA - Mindfulness and Social-Emotional Development: https://goodsensorylearning.com/collections/social-emotional-development - Executive Functioning publications at Good Sensory Learning: https://goodsensorylearning.com/collections/executive-functioning-skills-training - Executive Functioning Skills Workshop: https://www.learningspecialistcourses.com/courses/executive-functioning-skills-workshop Brought to you by - www.goodsensorylearning.com - www.learningspecialistcourses.com - www.bulletmapacademy.com

In episode 5 of WTS* we go over the HPA-axis. Topics include (but are not limited to) • what are hormones • The three classes: monoamines, peptides/proteins, and steroids • The anterior and posterior pituitary • The HPA axis and producing cortisol • The prefrontal cortex and the amygdala and how you can train your reactions • Today's FSF is the “Poop Bus” References: A. G. Watts. (2007). Anatomy of the HPA Axis (pg. 13-29). Nelson, R. J., & Kriegsfeld, L. J. (2018). An introduction to behavioral endocrinology. Sunderland, MA: Sinauer Associates. Hill, S. E. (2019). This is your brain on birth control: The surprising science of women, hormones, and the law of unintended consequences. NY, NY: Avery. UC Berkeley Courses Hormones and Behavior taught by Lance Kriegsfeld Ph.D, IBC143B Biological Clocks taught by Lance Kriegsfeld Ph.D, IBC143B Neurobiology of Stress taught by Daniela Kaufer Ph.D, IB139 Alex Honnold the solo climber https://nautil.us/issue/39/sport/the-strange-brain-of-the-worlds-greatest-solo-climber Pobody's Nerfect 26:05 — I say “inhibitory feedback” which is a technically incorrect. Inhibitory feedback is not a thing, in these events it's considered negative feedback which ends up causing inhibitory signals to whatever axis or pathway its acting on. 42:29 — I say voluntary actions which is misleading. What I mean is in terms of methodical actions of your own volition. For example, to pick up a cup is voluntary, but you don't really think about picking up the cup, this is not a prefrontal cortex (PFC) situation. However, to decide to quit a job would be something that your PFC would have been largely involved in and ultimately the master and commander of that action. 44:01 — I say “activation signals” with the amygdala to the hypothalamus its really “excitatory” and that creates activation. --- Send in a voice message: https://anchor.fm/ariel-castro6/message

รายการ สุขใจใกล้หมอ ใกล้หมอชะลอวัยกับหมอแอมป์ "ถั่งเช่า ดีจริงหรือไม่?" ตอนที่ 2 โดย หมอแอมป์ - นพ. ตนุพล วิรุฬหการุญ -ประธานเจ้าหน้าที่ปฏิบัติการ และ ผู้อำนวยการ BDMS Welness Clinic -ผู้อำนวยการ RoyalLife โรงพยาบาลกรุงเทพ -นายกสมาคมแพทย์ฟื้นฟูสุขภาพและส่งเสริมการศึกษาโรคอ้วน กรุงเทพ (BARSO) ออกอากาศทางช่อง PPTV HD 36 เมื่อ พ.ศ.2558 Keywords for Education: -Cordyceps Sinensis -Herbal Medicine -Lifestyle Medicine

รายการ สุขใจใกล้หมอ ใกล้หมอชะลอวัยกับหมอแอมป์ "ถั่งเช่า ดีจริงหรือไม่?" ตอนที่ 1 โดย หมอแอมป์ - นพ. ตนุพล วิรุฬหการุญ -ประธานเจ้าหน้าที่ปฏิบัติการ และ ผู้อำนวยการ BDMS Welness Clinic -ผู้อำนวยการ RoyalLife โรงพยาบาลกรุงเทพ -นายกสมาคมแพทย์ฟื้นฟูสุขภาพและส่งเสริมการศึกษาโรคอ้วน กรุงเทพ (BARSO) ออกอากาศทางช่อง PPTV HD 36 เมื่อ พ.ศ.2558 Keywords for Education: -Cordyceps Sinensis -Herbal Medicine -Lifestyle Medicine

On this episode of Sanity, Dr. Jason Duncan and Dr. Amanda Loerinc Guinyard discuss a new model of exposure treatment called the inhibitory learning model. Traditionally, exposure therapy was believed to work due to habituation, or the diminishing of a response to the feared or anxiety-provoking stimulus. Dr. Loerinc Guinyard describes how recent research suggests exposure therapy works because an individual is learning the previously feared stimuli no longer produces an anxiety response, known as the inhibitory learning model. Another aspect of this model includes an individual learning even if they are in an anxiety-provoking situation, they can tolerate and cope with those emotions. Positive Affect Treatment, a new therapy developed in part by Dr. Loerinc Guinyard, is also covered. This therapy is a transdiagnostic approach, meaning it can be useful for a number of different disorders, and its focus, not surprisingly, is on increasing positive emotional experiences, thoughts, and enhancing compassion. This is a great episode for those wanting to learn more about new therapeutic approaches and models! Resource: CBT Center of Boston: http://www.cbtcenterboston.com/ Concord Center in Massachusetts: https://www.concordcbt.com/ Treatments that Work Series https://global.oup.com/academic/content/series/t/treatments-that-work-ttw/?cc=us&lang=en& ABCT (Find a Therapist) https://www.findcbt.org/FAT/ Academy of Cognitive Therapy (Find a Therapist) https://www.academyofct.org/search/custom.asp?id=4410 Anything written by Michelle Craske: https://www.psych.ucla.edu/faculty-page/mcraske/ Social Media Information: Website: https://www.cbtcenterboston.com/about Instagram: @amandaloerincguinyard Vienna Beat by Blue Dot Sessions (www.sessions.blue)

Self-Control Skills   When there is a skill weakness in the executive function skill category it impacts learning and overall ability to achieve goals. It is important to identify in which skills group in this category is impacted in order to have a targeted equipping. Typically executive function skills are viewed as organizational and planning abilities. This skill group encompasses several mental processes that impact overall learning and social competency and is not limited to just organization and planning. We will define this skill group in detail.  In the process this will expand your understanding and assist you in improving you skill set in this area.  Cognitive (Self) Control "Executive Function" to Build Executive Function is a set of mental processes that have to do with managing oneself and one's resources in order to achieve a goal and involves mental control and self-regulation (Jericho, 2012); Working memory: holding information in mind while performing tasks Cognitive flexibility: to move freely from one situation to another and to think flexibly in order to respond appropriately to the situation (adapt) helps us to sustain or shift attention in response to different demands or to apply different rules in different settings Inhibitory control (includes self-control)  the ability to stop one's own behavior at the appropriate time, including stopping actions and thoughts enables us to set priorities and resist impulsive actions or responses Executive skills resulting from the above three processes (Rodden, 2020) : attention/focus: is sustained attention is the ability to maintain attention despite distractibility, fatigue or boredom abstract reasoning/concept formation/saliency determination: the ability to make connections, synthesize and categorize information. emotional regulation/control is the process of recognizing and controlling feelings or reactions to feelings (ability to modulate emotional responses by bringing rational thought to bear on feelings) self-monitoring is the ability to monitor and evaluate your own performance and to measure it against some standard of what is needed or expected task initiation is the ability to recognize when to get started on something and begin without procrastinating organization is the ability to create and maintain systems to keep track information and materials planning/prioritizing the ability to create steps to reach a goal and to make decisions about what to focus Thank you for listening please visit us at www.socialmindcenter.com for different skill notebook pages.  Work Cited Rodden, Janice. What is Executive Function Disorder? Additudemag. May 11, 2020; https://www.additudemag.com/what-is-executive-function-disorder- Jericho Schools. August, 2012. Executive Functioning: A Handbook for Grades K-12; http://www.jerichoschools.org/