FirstPersonScience

Why do cannabinoids in cannabis cause nausea and vomiting in some people but not others? Is this limited to heavy users, Recreational users, medicinal cannabis patients? In this episode, FPS ventures into the unknown on the very under-researched area of Cannabinoid Hyperemesis Syndrome. In this episode neuroscience PhD candidate Marieka Devuono joins us to speak about her recently published manuscript that addresses these controversial concepts, entitled "Conditioned gaping produced by high dose Δ9-tetrahydracannabinol: Dysregulation of the hypothalamic endocannabinoid system", published in Neurophamacology [2018 Oct;141:272-282. doi: 10.1016/j.neuropharm.2018.08.039]. Link: https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(18)30598-7 Highlights • High doses of THC produce nausea-induced conditioned gaping. • THC-induced conditioned gaping was mediated by its action on the CB1 receptor. • 10 mg/kg THC produced upregulation of genes related to the 2-AG degrading enzyme, MAGL in the hypothalamus. • High doses of THC may produce stress-induced nausea by dysregulation of endocannabinoid function in the hypothalamus. Abstract Δ9-tetrahydracannabinol (THC) is recognized as an effective treatment for nausea and vomiting via its action on the cannabinoid 1 (CB1) receptor. Paradoxically, there is evidence that THC can also produce nausea and vomiting. Using the conditioned gaping model of nausea in rats, we evaluated the ability of several doses of THC (0.0, 0.5, 5 and 10 mg/kg, i.p.) to produced conditioned gaping reactions. We then investigated the ability of the CB1 receptor antagonist, rimonabant, to block the establishment of THC-induced conditioned gaping. Real-time polymerase chain reaction (RT-PCR) was then used to investigate changes in endocannabinoid related genes in various brain regions in rats chronically treated with vehicle (VEH), 0.5 or 10 mg/kg THC. THC produced dose-dependent gaping, with 5 and 10 mg/kg producing significantly more gaping reactions than VEH or 0.5 mg/kg THC, a dose known to have anti-emetic properties. Pre-treatment with rimonabant reversed this effect, indicating that THC-induced conditioned gaping was CB1 receptor mediated. The RT-PCR analysis revealed an upregulation of genes for the degrading enzyme, monoacylglycerol lipase (MAGL), of the endocannabinoid, 2-arachidolyl glycerol (2-AG), in the hypothalamus of rats treated with 10 mg/kg THC. No changes in the expression of relevant genes were found in nausea (interoceptive insular cortex) or vomiting (dorsal vagal complex) related brain regions. These findings support the hypothesis that THC-induced nausea is a result of a dysregulated hypothalamic-pituitary-adrenal axis leading to an overactive stress response. Keywords THC Conditioned gaping Endocannabinoid system Hypothalamus Nausea. Use Filmora To Create Great Quality Videos - 20% off Link: http://tiny.cc/b86pkz ___________________________________________________________________________________ Interested in cutting-edge neuroscience research? Tired of exciting information being hidden behind those pesky paywalls? Introducing the First-Person Science Podcast: The 1st and only podcast dedicated to in-depth exploration of neuroscience research articles with first-hand perspectives and narratives from the authors themselves. FPS introduces a new way to discover and engage with neuroscience research. We aim to break-down barriers to science communication by explaining jargon and complicated concepts in entertaining and succinct ways in a ‘journal club’ style to encourage collaboration and discussion between scientists and the public, alike. Listeners can expect to learn cool facts and get a general background for everything related to the episode's journal article through a visually immersive ‘journal club’ approach to the podcast, Ft. narratives and first-person perspectives from the authors/scientists themselves. It's a fine line to manage, but we're doing our best! And the more feedback from people from all levels of background/understanding, the better! Listen to our podcast on itunes, spotify, or wherever you get your podcasts. Direct audio download link: https://firstpersonscience.podbean.com RSS Feed: https://feed.podbean.com/firstpersonscience/feed.xml Follow us on Twitter to stay up to date on the latest research: @firstpersonsci Facebook: https://www.facebook.com/First-Person-Science-106183617589132/ Instagram: https://www.instagram.com/firstpersonsciencepodcast/ Interested in increasing exposure for your published research? Curious about becoming involved with the show? Email us: firstpersonsciencepod@gmail.com. Produced by Roger Hudson, PhDc

Endocannabinoids - cannabinoids made in the body, by the body - are a Hot Topic in Neuroscience & Beyond - with Western & integrative medicine coming to embrace the role of these important compounds, the EndoCannabinoid system is emerging as a therapeutic target for treatment of several psychiatric disorders. However, endocannabinoid system research is limited by scientists' ability to translate these groundbreaking research discoveries into clinical treatments, mostly due to a lack of understanding of how this system is involved with basic physiological processes, including stress & anxiety. In this episode, Dr. David Marcus - A recent graduate of the Neuroscience PhD Program at Vanderbilt University & 1st author of this episode's manuscript - joins us to speak about the recently published manuscript, "Endocannabinoid Signaling Collapse Mediates Stress-Induced Amygdalo-Cortical Strengthening", published in the journal Neuron. https://www-sciencedirect-com.proxy1.lib.uwo.ca/science/article/pii/S0896627319310906 Highlights • The BLA-plPFC circuit is engaged by stress exposure and its activation is anxiogenic •Stress enhances glutamate release in a reciprocal BLA-plPFC-BLA subcircuit •BLA-plPFC glutamatergic drive is constrained by multimodal 2-AG signaling •2-AG signaling collapse mediates stress-induced circuit strengthening and anxiety Abstract Functional coupling between the amygdala and the dorsomedial prefrontal cortex (dmPFC) has been implicated in the generation of negative affective states; however, the mechanisms by which stress increases amygdala-dmPFC synaptic strength and generates anxiety-like behaviors are not well understood. Here, we show that the mouse basolateral amygdala (BLA)-prelimbic prefrontal cortex (plPFC) circuit is engaged by stress and activation of this pathway in anxiogenic. Furthermore, we demonstrate that acute stress exposure leads to a lasting increase in synaptic strength within a reciprocal BLA-plPFC-BLA subcircuit. Importantly, we identify 2-arachidonoylglycerol (2-AG)-mediated endocannabinoid signaling as a key mechanism limiting glutamate release at BLA-plPFC synapses and the functional collapse of multimodal 2-AG signaling as a molecular mechanism leading to persistent circuit-specific synaptic strengthening and anxiety-like behaviors after stress exposure. These data suggest that circuit-specific impairment in 2-AG signaling could facilitate functional coupling between the BLA and plPFC and the translation of environmental stress to affective pathology. Keywords 2-arachidonoylglycerol, glutamate, prefrontal cortex, anxiety, cannabinoid, amygdala, stress, optogenetics, cannabis, post traumatic stress disorder. Interested in cutting-edge neuroscience research? Tired of exciting information being hidden behind those pesky paywalls? Introducing the First-Person Science Podcast: The 1st and only podcast dedicated to in-depth exploration of neuroscience research articles with first-hand perspectives and narratives from the authors themselves. FPS introduces a new way to discover and engage with neuroscience research. We aim to break-down barriers to science communication by explaining jargon and complicated concepts in entertaining and succinct ways in a ‘journal club’ style to encourage collaboration and discussion between scientists and the public, alike. In each episode, a scientist joins the show to speak about their recent ‘first-author’ manuscript. We walk viewers through each figure “1 bar graph at a time” using panel-to-panel summaries with video and visual illustrations to aid understanding of complex topics. View all figures and aspects of the research articles on our YT channel: youtube.com/firstpersonsciencepodcast Listeners can expect to learn cool facts and get a general background for everything related to the episode's journal article through a visually immersive ‘journal club’ approach to the podcast, Ft. narratives and first-person perspectives from the authors/scientists themselves. It's a fine line to manage, but we're doing our best! And the more feedback from people from all levels of background/understanding, the better! Listen to our podcast on itunes, spotify, or wherever you get your podcasts. Direct audio download link: https://firstpersonscience.podbean.com RSS Feed: https://feed.podbean.com/firstpersonscience/feed.xml Follow us on Twitter to stay up to date on the latest research: @firstpersonsci Facebook: https://www.facebook.com/First-Person-Science-106183617589132/ Instagram: https://www.instagram.com/firstpersonsciencepodcast/ Interested in increasing exposure for your published research? Curious about becoming involved with the show? Email us: firstpersonsciencepod@gmail.com. Produced by Roger Hudson, PhDc

The discovery of biomarkers related to depression and other psychiatric disorders have been accelerated in recent years due to emphasis on genomics and proteomics research, Precision medicine (or personalized medicine), and collaborative approaches across research labs. Using knowledge of these biomarkers, scientists are better able to identify of those with genetic predispositions, as well as improve diagnosis, treatment, and prognosis for those with depression (MDD). In this episode neuroscience PhD candidate, Stephen Daniels, joins us to speak about his recently published manuscript that addresses these controversial concepts, entitled "Reverse Translation of Major Depressive Disorder Symptoms: A Framework for the Behavioural Phenotyping of Putative Biomarkers", published in The Journal of Affective Disorders [2020 Feb; 263(15): 353-366] / DOI: 10.1016/j.jad.2019.11.108. https://www.sciencedirect.com/science/article/abs/pii/S0165032719325510 Highlights • Reverse translation of biomarkers of depression. • Basic bio-behavioural functions in humans and animals. • Battery of tests in animals to study clinical biomarkers. Abstract Background Reverse translating putative biomarkers of depression from patients to animals is complex because Major Depressive Disorder (MDD) is a highly heterogenous condition. This review proposes an approach to reverse translation based on relating relevant bio-behavioural functions in laboratory rodents to MDD symptoms. Methods This systematic review outlines symptom clusters assessed by psychometric tests of MDD and antidepressant treatment response including the Montgomery–Åsberg Depression Rating Scale, the Hamilton Depression Rating Scale, and the Beck Depression Inventory. Symptoms were related to relevant behavioural assays in laboratory rodents. Results The resulting battery of tests includes passive coping, anxiety-like behaviours, sleep, caloric intake, cognition, psychomotor functions, hedonic reactivity and aversive learning. These assays are discussed alongside relevant clinical symptoms of MDD, providing a framework through which reverse translation of a biomarker can be interpreted. Limitations Certain aspects of MDD may not be quantified by tests in laboratory rodents, and their biological significance may not always be of clinical relevance. Conclusions Using this reverse translation approach, it is possible to clarify the functional significance of a putative biomarker in rodents and hence translate its contribution to specific clinical symptoms, or clusters of symptoms. Keywords Major depressive disorder, Montgomery–Åsberg depression rating scale, Hamilton rating scale for depression, Beck Depression inventory Use Filmora To Create Great Quality Videos - 20% off Link: http://tiny.cc/b86pkz ___________________________________________________________________________________ Interested in cutting-edge neuroscience research? Or cutting through the ribbons of public-accessibility for research articles? Introducing the First-Person Science Podcast: The 1st and only podcast dedicated to in-depth exploration of neuroscience research articles with first-hand perspectives and narratives from the authors themselves. FPS introduces a new way to discover and engage with neuroscience research. We aim to break-down barriers to science communication by explaining jargon and complicated concepts in entertaining and succinct ways in a ‘journal club’ style to encourage collaboration and discussion between scientists and the public, alike. In each episode, a scientist joins the show to speak about their recent ‘first-author’ manuscript. We walk viewers through each figure “1 bar graph at a time” using panel-to-panel summaries with video and visual illustrations to aid understanding of complex topics. View all figures and aspects of the research articles on our YT channel: https://www.youtube.com/channel/UCxIStqpo1YZRTFKn5m1J0iQ Listeners can expect to learn cool facts and get a general background for everything related to the episode's journal article through a visually immersive ‘journal club’ approach to the podcast, Ft. narratives and first-person perspectives from the authors/scientists themselves. It's a fine line to manage, but we're doing our best! And the more feedback from people from all levels of background/understanding, the better! Listen to our podcast on itunes, spotify, or wherever you get your podcasts. Direct audio download link: https://firstpersonscience.podbean.com RSS Feed: https://feed.podbean.com/firstpersonscience/feed.xml Follow us on Twitter to stay up to date on the latest research: @firstpersonsci Facebook: https://www.facebook.com/First-Person-Science-106183617589132/ Interested in increasing exposure for your published research? Curious about becoming involved with the show? Email us: firstpersonsciencepod@gmail.com. Produced by Roger Hudson, PhDc

Addictive drugs are said to often worsen memory, and anecdotal reports of drug-users with poor memory are abundant. But what if these reports are wrong? What if drugs of abuse can improve memory under particular circumstances? In this episode, Michael Wolter - Neuroscience PhD Candidate from the University of Guelph - joins us to discuss how Heroin and other drugs of abuse (including cocaine & nicotine) can enhance memory for events immediately preceding drug intake. This work has vast implications for the development of addiction, and for preventing relapse to addictive drugs. In fact, drug-linked experiences stored in the brain's long-term memory centres are believed to be largely responsible for relapse to drug seeking behaviour and drug abuse, even after long periods of successful abstinence. Manuscript: Modulation of object memory consolidation by Heroin and Heroin-conditioned stimuli: Role of opioid and noradrenergic systems. Published in the journal European Neuropsychopharmacology: https://www.ncbi.nlm.nih.gov/pubmed/32067860 Abstract There is recent evidence that cocaine, nicotine, and their conditioned stimuli have the ability to enhance memory consolidation. The present study compared the effects of post-training Heroin and of a drug-paired contextual conditioned stimulus (CS+) on consolidation of object recognition memory and investigated the roles of opioid and beta-adrenergic receptors in Heroin/CS+ memory modulation by co-administering the respective antagonists, naltrexone (NTX) and propranolol (PRO). Three experiments were performed in male Sprague-Dawley rats demonstrating that immediate, but not delayed, post-sample exposure to Heroin (0.3, 1 mg/kg), or exposure (30 min) to a contextual CS+ paired with 1 mg/kg Heroin (5 pairings, each 120 min), equally enhanced object memory. Importantly, while the memory enhancing effects of 1 mg/kg Heroin and of the contextual CS+ were not altered by post-training co-administration of 3 mg/kg naltrexone, they were blocked by post-training co-administration of 10 mg/kg propranolol. Taken together, these data suggest that a context paired with Heroin shares the memory enhancing effect of Heroin itself and that these unconditioned and conditioned drug stimuli may modulate memory through the activation of beta-noradrenergic receptors. KEYWORDS: Conditioned stimulus; Heroin; Memory consolidation; Naltrexone; Object recognition; Propranolol Use Filmora To Create Great Quality Videos - 20% off Link: http://tiny.cc/b86pkz ___________________________________________________________________________________ Interested in cutting-edge neuroscience research? Tired of exciting information being hidden behind those pesky paywalls? Introducing the First-Person Science Podcast: The 1st and only podcast dedicated to in-depth exploration of neuroscience research articles with first-hand perspectives and narratives from the authors themselves. FPS introduces a new way to discover and engage with neuroscience research. We aim to break-down barriers to science communication by explaining jargon and complicated concepts in entertaining and succinct ways in a 'journal club' style to encourage collaboration and discussion between scientists and the public, alike. In each episode, a scientist joins the show to speak about their recent 'first-author' manuscript. We walk viewers through each figure "1 bar graph at a time" using panel-to-panel summaries with video and visual illustrations to aid understanding of complex topics. Listeners can expect to learn cool facts and get a general background for everything related to the episode's journal article through a visually immersive 'journal club' approach to the podcast, Ft. narratives and first-person perspectives from the authors/scientists themselves. It's a fine line to manage, but we're doing our best! And the more feedback from people from all levels of background/understanding, the better! Listen to our podcast on itunes, spotify, or wherever you get your podcasts. Direct audio download link: https://firstpersonscience.podbean.com RSS Feed: https://feed.podbean.com/firstpersons... Follow us on Twitter to stay up to date on the latest research: @firstpersonsci Facebook: https://www.facebook.com/First-Person... Instagram: https://www.instagram.com/firstperson... Interested in increasing exposure for your published research? Curious about becoming involved with the show? Email us: firstpersonsciencepod@gmail.com. Sources for Further Education & Reading: https://online-learning.harvard.edu/course/fundamentals-neuroscience-part-2-neurons-and-networks?delta=0

In this episode, we discuss the mechanisms that regulate microglia phagocytosis (such as TRPV2 and other vanilloid receptors) - AKA eating apoptosis ready cells - and how the brain maintains healthy function in aging and after injury, such as traumatic brain injury (TBI).Because neurons get all the attention, you don't hear too much about glia. Although glia cells DO NOT carry nerve impulses (action potentials) they do have many important functions. In fact, without glia, the neurons would not work properly! Neuroscience PhD Candidates Matthew Maksoud and Viki Tellios join us to speak on their article - Nitric Oxide Upregulates microglia phagocytosis and increases transient receptor potential vanilloid type 2 channel expression on the plasma membrane - published in the journal Glia: https://onlinelibrary.wiley.com/doi/full/10.1002/glia.23685 Abstract Microglia phagocytosis is critical for central nervous system development, and dysregulation of phagocytosis may contribute to a variety of neurological disorders. During initial stages of phagocytosis, microglia display increased nitric oxide (NO) production via inducible nitric oxide synthase (iNOS) activity and amplified calcium entry through transient receptor potential vanilloid type 2 (TRPV2) channels. The present study investigated the regulatory role of iNOS/NO signaling in microglial phagocytosis and TRPV2 channel activation using phagocytosis assay, calcium imaging, patch clamp electrophysiology, immunocytochemistry, and immunoblot assays. Results showed that primary microglia from iNOS‐knockout (iNOS−/−) mice exhibited substantial deficits in phagocytic capacity and TRPV2 channel activity relative to wild‐type (WT) controls. Specifically, iNOS−/− microglia displayed a lower level of TRPV2 protein localized on the plasma membrane (PM) without any significant change in the mRNA levels of Fc‐gamma receptors and TRPV2. In addition, iNOS−/− microglia, unlike their WT controls, failed to elicit a calcium influx in response to application of the TRPV2‐agonist 2‐aminoethoxydiphenyl borate (2APB). Importantly, the phagocytic capacity and the PM expression and activity of TRPV2 in iNOS−/− microglia were largely corrected by pretreatment with NO‐donors. Accordingly, the 2APB‐evoked calcium influx and the PM expression of TRPV2 in WT microglia were significantly decreased by selective inhibition of iNOS, protein kinase‐G (PKG), or phosphoinositide‐3‐kinase (PI3K), respectively. Together, results from this study indicated that iNOS/NO signaling upregulates microglial phagocytosis and increases TRPV2 trafficking to the PM via PKG/PI3K dependent pathway(s) and vanilloid receptors. Use Filmora To Create Great Quality Videos - 20% off Link: http://tiny.cc/b86pkz ___________________________________________________________________________________ Interested in cutting-edge neuroscience research? Tired of exciting information being hidden behind those pesky paywalls? Introducing the First-Person Science Podcast: The 1st and only podcast dedicated to in-depth exploration of neuroscience research articles with first-hand perspectives and narratives from the authors themselves. FPS introduces a new way to discover and engage with neuroscience research. We aim to break-down barriers to science communication by explaining jargon and complicated concepts in entertaining and succinct ways in a 'journal club' style to encourage collaboration and discussion between scientists and the public, alike. In each episode, a scientist joins the show to speak about their recent 'first-author' manuscript. We walk viewers through each figure "1 bar graph at a time" using panel-to-panel summaries with video and visual illustrations to aid understanding of complex topics. Listeners can expect to learn cool facts and get a general background for everything related to the episode's journal article through a visually immersive 'journal club' approach to the podcast, Ft. narratives and first-person perspectives from the authors/scientists themselves. It's a fine line to manage, but we're doing our best! And the more feedback from people from all levels of background/understanding, the better! Listen to our podcast on itunes, spotify, or wherever you get your podcasts. Direct audio download link: https://firstpersonscience.podbean.com RSS Feed: https://feed.podbean.com/firstpersons... Follow us on Twitter to stay up to date on the latest research: @firstpersonsci Facebook: https://www.facebook.com/First-Person... Instagram: https://www.instagram.com/firstperson... Interested in increasing exposure for your published research? Curious about becoming involved with the show? Email us: firstpersonsciencepod@gmail.com

The amygdala is a prominent brain region known for its involvement in learning and memory in emotional situations including during fear, anxiety, and pleasure - including its activation in the fight or flight response. However, this psychology related research has taken place almost exclusively in laboratory environments with limited ability to generalize to natural settings that rodents would be instinctually prepared to learn in. How the amygdala processes this information in more natural environments has not been explored. In Episode #3 of First-Person Science, PhD Candidate Peter Zambetti from the University of Washington speaks on his recently published manuscript in iScience. Using instinctual fear stimuli (a 3D owl) rather than the classic foot-shock, Dr. Zambetti aims to better understand innate defensive behaviors. "S*ex Differences in Foraging Rats to Naturalistic Aerial Predator Stimuli", published in iScience from CellPress [Volume 16, 28 June 2019, Pages 442-452] / DOI:10.1016/j.isci.2019.06.011. Open Access Article link: https://www.sciencedirect.com/science/article/pii/S2589004219301932 Manuscript Abstract: Rodents in the wild are under nearly constant threat of aerial predation and thus have evolved adaptive innate defensive behaviors, such as freezing or fleeing, in response to a perceived looming threat. Here we employed an ethologically relevant paradigm to study innate fear of aerial predators in male and female rats during a goal-oriented task. Rats foraging for food in a large arena encountered either a 2D or 3D looming stimulus, to which they instinctively fled back to a safe nest. When facing a direct aerial threat, female rats exhibited a greater fear response than males and this divergence maintained when exposed to the environment on subsequent days with no predator interaction, suggesting stronger contextual fear in female rats. These results may have relevance toward exploring neurobiological mechanisms associated with higher diagnosis rates of fear and anxiety-related disorders in women as compared with men. Highlights • Female rats exhibited stronger fear responses to aerial threats than male rats • A 3D aerial predator was more effective at eliciting fear responses than 2D stimuli • Contextual fear memories were formed from repeated 3D predator exposures Use Filmora To Create Great Quality Videos - 20% off Link: http://tiny.cc/b86pkz ___________________________________________________________________________________ Interested in cutting-edge neuroscience research? Or cutting through the ribbons of public- accessibility for research articles? Introducing First-Person Science: the first and only podcast dedicated to in-depth exploration of neuroscience research articles with first-hand perspectives and narratives from the authors themselves. FPS introduces a new way of discovering and engaging with neuroscience-based research, and breaks down barriers to science communication that will encourage collaboration and discussion between scientists and the public, alike. In each episode, an FPS host interviews a scientist about their recent ‘first-author’ manuscript, walking listeners/viewers through figures and tables “1 bar graph at a time” with point-by-point visuals, figure illustrations, and summaries for those interested or without access to the research articles, or both. YT channel: https://www.youtube.com/channel/UCxIStqpo1YZRTFKn5m1J0iQ FPS aims to be relevant and interesting to both neuroscience experts and those without science backgrounds by breaking down jargon and complicated concepts in entertaining and succinct ways. Listeners can expect to learn learn cool facts and get a general background for everything to do with the episode's chosen journal article in ~35 mins or less via an audio-book style interview-podcast, but for journal articles, with narratives and first-person perspectives from the authors/scientists themselves. It's a fine line to manage, but we're doing our best! And the more feedback from people from all levels of background/understanding, the better! Listen on itunes, spotify, or wherever you get your podcasts. Direct audio download link: https://firstpersonscience.podbean.com/ Having a hard time following along with the audio? Check out our YouTube channel with point-by-point visuals, figure illustrations, and summaries for those interested or without access to the research articles, or both! https://www.youtube.com/channel/UCxIStqpo1YZRTFKn5m1J0iQ Follow us on Twitter to stay up to date on the latest research: @firstpersonsci Facebook: https://www.facebook.com/First-Person-Science-106183617589132/ Interested in increasing exposure for your published research? Curious about becoming involved with the show? Email us: firstpersonsciencepod@gmail.com. Produced by Roger Hudson, PhDc

Evidence suggests that THC and CBD each act on specific receptors in the brain to cause different effects on Biomarkers, other neurotransmitter systems and molecular pathways. In fact, CBD can even prevent many of the side effects associated with potent cannabis (high THC cannabis) such as psychosis, paranoia, and in some cases can act as a treatment for those diagnosed with schizophrenia. In this episode of First-Person Science, PhD Candidate & Vanier Scholar Roger Hudson speaks about his recently published manuscript in the Journal Of Neuroscience, discussing how THC causes adverse psychiatric side-effects in some users, and the science of how cannabidiol (CBD) can counteract these side effects. "Cannabidiol (CBD) Counteracts the Psychotropic Side-Effects of Delta-9-Tetrahydrocannabinol (THC) in the Ventral Hippocampus through Bidirectional Control of ERK1–2 Phosphorylation", published in The Journal of Neuroscience [2019 Oct;39(44):8762–8777] / DOI:10.1523/JNEUROSCI.0708-19.2019. https://www.ncbi.nlm.nih.gov/pubmed/31570536 _________________________________________________________________________________ Use Filmora To Create Great Quality Videos - 20% off Link: http://tiny.cc/b86pkz ABSTRACT: Evidence suggests that the phytocannabinoids Delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) differentially regulate salience attribution and psychiatric risk. The ventral hippocampus (vHipp) relays emotional salience via control of dopamine (DA) neuronal activity states, which are dysregulated in psychosis and schizophrenia. Using in vivo electrophysiology in male Sprague Dawley rats, we demonstrate that intra-vHipp THCstrongly increases ventral tegmental area (VTA)DAneuronal frequency and bursting rates, decreases GABA frequency, and amplifies VTA beta, gamma and epsilon oscillatory magnitudes via modulation of local extracellular signal-regulated kinase phosphorylation (pERK1–2). Remarkably, whereas intra-vHipp THC also potentiates salience attribution in morphine place-preference and fear conditioning assays, CBD coadministration reverses these changes by downregulating pERK1–2 signaling, as pharmacological reactivation of pERK1–2 blocked the inhibitory properties of CBD. These results identify vHipp pERK1–2 signaling as a critical neural nexus point mediating THC-induced affective disturbances and suggest a potential mechanism by which CBD may counteract the psychotomimetic and psychotropic side effects of THC. Keywords: cannabidiol; delta-9-tetrahydrocannabinol; dopamine; extracellular signal-regulated kinase; ventral hippocampus; ventral tegmental area. ___________________________________________________________________________________ Interested in cutting-edge neuroscience research? Or cutting through the ribbons of public- accessibility for research articles? Introducing First-Person Science: the first and only podcast dedicated to in-depth exploration of neuroscience research articles with first-hand perspectives and narratives from the authors themselves. First-Person Science introduces a new way of discovering and engaging with neuroscience-based research, and breaks down barriers to science communication that will encourage collaboration and discussion between scientists and the public, alike. The podcast aims to be relevant to neuroscience experts and the public, alike - to serve a role similar to an audio-book, but for journal articles, and with a much-enhanced experience. We aim to explain jargon and complicated concepts in a brief/succinct way so that first-time listeners can easily understand, while simultaneously not boring those that are experts in the field. Listen to our podcast on itunes, spotify, or wherever you get your podcasts. Direct audio download link: https://firstpersonscience.podbean.com/ Follow us on Twitter to stay up to date on the latest research: @firstpersonsci Interested in increasing exposure for your published research? Curious about becoming involved with the show? Email us: firstpersonsciencepod@gmail.com. Produced by Roger Hudson, PhDc

In this inaugural release of First-Person Science, Roger Hudson speaks with Thomas Lapointe about his recently published manuscript that explores the behavioural and brain mRNA effects of combined escitalopram (an SSRI; antidepressant) and adjunct aripiprazole (5-HT1a agonist) in rats, with a specific focus on the 5-HT1a receptor. This podcast also discusses how scientists are enhancing the therapeutic efficacy of antidepressants and some of the mechanisms involved. "Effects of combined escitalopram and aripiprazole in rats: role of the 5-HT1a receptor", published in Psychopharmacology [2019 Jul;236(7):2273-2281] / DOI:10.1007/s00213-019-05225-z. https://link.springer.com/article/10.1007/s00213-019-05225-z Manuscript Abstract: RATIONALE: Pre-clinical and clinical studies have suggested that the antidepressant efficacy of escitalopram (ESC) can be augmented by co-administration of aripiprazole (ARI). OBJECTIVE: To establish if the effects of ESC + ARI can be altered by modulating the 5-HT1a receptor. METHODS: Sprague-Dawley male rats received ESC + ARI (10 and 2 mg/kg/day, respectively, via osmotic or by cumulative injections), as well as the 5-HT1a antagonist WAY-100635 (WAY; 0.01-1 mg/kg) and the 5-HT1a agonist 8-OH-DPAT (DPAT; 0.3-1 mg/kg) prior to testing in locomotion chambers and in the forced swim test (FST). Expression of the 5-HT1a receptor mRNA in the dorsal raphe nucleus, hippocampus, septum, and entorhinal cortex was also assessed. RESULTS: WAY generally synergized, while DPAT antagonized, the effect of ESC + ARI on motor activity. All groups showed significantly lower 5-HT1a mRNA in the dorsal raphe nucleus. In the hippocampus, ESC + ARI and WAY + ESC + ARI groups displayed equivalent elevations of 5-HT1a mRNA, but this was not observed in groups that received DPAT + ESC + ARI. Finally, the addition of ARI to ESC augmented the effect that ESC alone had on reducing immobility in the FST. Importantly, WAY antagonized this effect, while DPAT had no consequences. CONCLUSIONS: Taken together, these results in rats indicate that the 5-HT1a receptor is involved in the behavioral and brain region-specific mRNA effects of ESC + ARI. KEYWORDS: 5-HT1a receptor; Antidepressant; Aripiprazole; Augmentation; Depression; Escitalopram; Forced swim; Psychomotor; SSRI; mRNA Use Filmora To Create Great Quality Videos - 20% off Link: http://tiny.cc/b86pkz _______________________________________________________________________ First-Person Science is the first and only Webcast dedicated to in-depth exploration of scientific research articles w/ first-hand perspectives & narratives from the authors themselves. We aim to increase promotion of neuroscience research articles and provide exposure for the scientists behind the work, as well as enhance public accessibility to publicly-funded, cutting-edge research. Hosted/Produced by Roger Hudson & Thomas Lapointe