{"title":"The Pharmacological Profile of Plant-Derived Cannabinoids In Vitro.","authors":"Stephen P H Alexander","doi":"10.1007/7854_2025_605","DOIUrl":"https://doi.org/10.1007/7854_2025_605","url":null,"abstract":"<p><p>With over 100 apparently unique metabolites in the Cannabis plant, there are a plethora of potential molecular targets. The molecular actions of Δ<sup>9</sup>-tetrahydrocannabinol are the best-investigated, which have centred mostly on a relatively high-potency, low-efficacy action at the CB<sub>1</sub> cannabinoid receptor. By contrast, cannabidiol has a multitude of lower potency molecular targets identified in vitro, but with limited clarity about their relevance for the effects of cannabidiol in humans. This review highlights the incomplete nature of studies of the major phytocannabinoids, particularly the acid phytocannabinoids.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145257746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Psychedelic-Associated Depersonalization-Derealization Disorder.","authors":"Matthias Michal","doi":"10.1007/7854_2025_599","DOIUrl":"https://doi.org/10.1007/7854_2025_599","url":null,"abstract":"<p><p>Depersonalization (DP) and Derealization (DR) refer to perceptual changes of \"as-if-character\" where the self (→DP) or the surroundings (→DR) are experienced as unreal. These symptoms are highly prevalent in individuals with mental disorders. If these symptoms persist most of the day for months, the diagnosis of depersonalization-derealization-disorder (DDD) is likely. DDD is a common disorder with a high comorbidity with depression, anxiety disorders, and personality disorders.The intake of classic psychedelic drugs often elicits DP/DR symptoms, which cease in most cases when the drug is eliminated. DDD is frequently precipitated by drug intoxication (cannabis and classic psychedelics). Patients and some researchers assume, therefore, that drug intoxication is the cause of DDD and frame it as a \"never-ending trip.\" Researchers base their assumption on the potential of psychedelics to elicit DP/DR symptoms and on case series of individuals reporting long-lasting uncomfortable symptoms after drug intake. Arguments are presented that demonstrate this is a reductionist conclusion and that this assertion may lead to false illness perceptions, hinder awareness of emotional conflicts, and erode patients' self-efficacy. The main arguments are that, first, DDD is a mental disorder resulting from the avoidance of aversive emotional states. DDD is related to functional alterations of brain networks rather than organic brain damage. Second, psychedelics act as a catalyst that accelerates the onset of DDD in vulnerable individuals by mobilizing complex anxiety-laden unconscious emotions from early attachment traumas.The treatment of DDD encompasses psychoeducation about the nature of the disorder, challenging false causal attributions to external causes (such as drug intake) and helping the patient experience and process their emotions adaptively. To achieve remission, patients usually need long-term psychotherapy of 50-100 sessions.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Michaela A Pettie, Linda C M Wilkin-Krug, Bart Ellenbroek
{"title":"Pre- and Postnatal Valproate Exposure Affects Brain Development.","authors":"Michaela A Pettie, Linda C M Wilkin-Krug, Bart Ellenbroek","doi":"10.1007/7854_2025_603","DOIUrl":"https://doi.org/10.1007/7854_2025_603","url":null,"abstract":"<p><p>This review investigates the teratogenic impact of valproic acid (VPA) on brain development, focusing on dose-dependent and timing-related behavioural and neurological outcomes in rats and mice, with an emphasis on using it as a model for autism spectrum disorders (ASD). Single and multiple administration methods (e.g., oral gavage and intraperitoneal injections) across various rat and mouse strains consistently report behavioural alterations (i.e., altered social interaction and locomotor activity) and neuronal changes, particularly in the hippocampus and cerebellum. We underscore the importance of understanding dose-related changes and the critical role of VPA exposure in determining the long-term neurodevelopmental effects. While animal models provide valuable insights into the pre- and postnatal effects of drug exposure, this chapter also addresses the limitation of extrapolating such findings to humans given the face and construct validity of the model. Overall, this review emphasises VPA's utility in modelling ASD-like behaviours and the need for ongoing research to refine these models for better applicability to humans.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mayerli A Prado Rivera, Joëlle D Jagersma, Jocelien D A Olivier
{"title":"Maternal SSRI Use During Pregnancy: Links Between Gut Microbiome, Offspring Behaviour, and Brain Transcriptomics.","authors":"Mayerli A Prado Rivera, Joëlle D Jagersma, Jocelien D A Olivier","doi":"10.1007/7854_2025_602","DOIUrl":"https://doi.org/10.1007/7854_2025_602","url":null,"abstract":"<p><p>Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed to treat maternal depression during pregnancy, yet their potential impact on foetal brain development remains a concern. Although maternal illness is a known confounder, growing evidence from both clinical and preclinical studies suggests that perinatal SSRI exposure may independently influence neurodevelopmental outcomes. This review draws on rodent studies to explore how developmental SSRI exposure affects the gut microbiome, maternal behaviour, myelination, and offspring social behaviour. Elevated serotonin levels caused by SSRIs can alter both brain development and the maternal gut microbiota, with possible long-term effects on offspring. Behaviourally, SSRI-exposed offspring often show reduced social play, altered social interactions, and sex-specific effects on aggression and sexual behaviour, in which males appear more sensitive to these effects than females. Maternal care is only modestly affected. Overall, developmental SSRI exposure in the absence of maternal illness can disrupt brain development and social behaviour in offspring, potentially through gut-brain axis mechanisms and altered myelination.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H M Harris, C F Moore, B W Jenkins, M F Bedillion, E M Weerts, C A Arout
{"title":"Delta-9-tetrahydrocannabinol and Cannabidiol for Pain: Preclinical and Clinical Models.","authors":"H M Harris, C F Moore, B W Jenkins, M F Bedillion, E M Weerts, C A Arout","doi":"10.1007/7854_2025_604","DOIUrl":"https://doi.org/10.1007/7854_2025_604","url":null,"abstract":"<p><p>Cannabinoids are increasingly being used to manage pain resulting from a variety of conditions. Both preclinical animal models and human studies have played a crucial role in advancing our knowledge of cannabinoids, their involvement in pain mechanisms, and their potential utility as novel analgesics. This chapter first reviews basic pain neurobiology and the most common experimental pain paradigms, which provide a basis for our discussion of preclinical, human laboratory, and clinical research characterizing the effectiveness of cannabinoids for managing pain. While a substantial body of literature exists describing these effects, findings are complex and largely mixed, dependent on the cannabinoid administered, route of administration, and pain modality/syndrome tested. Herein, we highlight the need for more rigorous, placebo-controlled research defining the therapeutic efficacy of cannabinoids. The chapter concludes by emphasizing the need for further investigation of other cannabis constituents (e.g., minor cannabinoids and terpenes), potential interactions between cannabinoids and other analgesic medications, as well as other emerging issues in the intersection between cannabinoids and pain management.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Functional Consequences Paternal Preconceptual Alcohol Consumption.","authors":"Sahir Hussain, Darren Day, Bart Ellenbroek","doi":"10.1007/7854_2025_601","DOIUrl":"https://doi.org/10.1007/7854_2025_601","url":null,"abstract":"<p><p>Alcohol is the most harmful drug of abuse, making alcoholism a major economic and public health crisis. Unsurprisingly, this has led to the majority of the neurobiological research on alcohol focusing on its direct effects on an individual, including those affected by foetal alcohol spectrum disorders (FASDs). However, research has shown that heavy paternal drinking predicts earlier and heavier adolescent drinking in the offspring, accompanied by other behavioural and molecular changes. While alcohol use disorder (AUD) is highly heritable, research on genetic variants alone does not sufficiently account for AUD risk and the FASDs-like symptoms seen in offspring of alcoholic fathers. Recently, there has been an increase in appreciation of the importance of epigenetic mechanisms of inheritance, which transfer changes due to parental experiences through the germline. This chapter aims to present an overview of the current knowledge on the inter- and transgenerational impacts of preconceptual paternal alcohol consumption (PPAC), the outcomes seen across generations and the mechanisms by which these changes may be passed down generations.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Acute Effects and Long-Term Neuropsychological Consequences of Classic Psychedelics Use.","authors":"Lukas Andreas Basedow, Thomas Günther Riemer","doi":"10.1007/7854_2025_600","DOIUrl":"https://doi.org/10.1007/7854_2025_600","url":null,"abstract":"<p><p>Psychedelics are gaining attention for their potential as therapeutic adjuncts for the treatment of psychological disorders. Additionally, the recreational use of these substances has been rising for the past years. In the context of a comprehensive analysis of potential harms induced by these substances, concerns regarding the cognitive and neuropsychological impact of their use remain. This chapter explores the acute, subacute, and long-term neuropsychological consequences of psychedelic use. Studies show that neuropsychological performance, especially attention and working memory, is reduced under the influence of a psychedelic. While not harmful in itself, this effect poses potential risks when combined with high-risk environments, such as road traffic. While these acute impairments seem to disappear on the day after psychedelic use, there is limited evidence that some impairments in executive functioning can persist for up to 24 h. Thus, caution is not only warranted during psychedelic use but also for the following day. In contrast, psychedelics do not seem to induce persistent changes in neuropsychological performance through repeated use, indicating no direct neuropsychological harms. However, further research is required to clarify the differential effects of various psychedelic substances and to assess the impact of chronic use across different contexts.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144946643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Future of Perceptual Dysregulation in Psychiatric Nosology.","authors":"Albert R Powers, Sahib S Khalsa","doi":"10.1007/7854_2025_596","DOIUrl":"https://doi.org/10.1007/7854_2025_596","url":null,"abstract":"<p><p>Like other medical illnesses, psychiatric conditions are defined by the presence of characteristic signs and symptoms that cause distress and dysfunction. Unlike most medical illnesses, however, the pathophysiological mechanisms underlying psychiatric symptoms remain largely unknown. Recent work in theory-driven computational neuroscience has proposed a unified account of how organisms derive estimates of both external and internal states by integrating prior beliefs with sensory input. This framework offers a powerful means of explaining typical perception and action, while also identifying how these processes may go awry to produce a panoply of psychiatric symptoms. Disruptions in this inferential process, which we term perceptual dysregulation, span exteroceptive, proprioceptive, and interoceptive systems and manifest across conditions ranging from psychosis and autism to anxiety and trauma-related disorders, functional neurological disorder, and dementia. This volume reviews emerging evidence for maladaptive sensory inference across psychiatric and neurological illness and explores how computational models based on Bayesian statistics can illuminate shared mechanisms beneath diverse symptom presentations. We argue that targeting perceptual dysregulation may not only enable new interventions but also catalyze the development of a revised psychiatric nosology grounded in testable models of brain-body interaction.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144820882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Correction to: Genetic Tools in Rodents to Study Cannabinoid Functions.","authors":"Krisztina Monory, Inigo Ruiz de Azua, Beat Lutz","doi":"10.1007/7854_2025_584","DOIUrl":"https://doi.org/10.1007/7854_2025_584","url":null,"abstract":"","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144793765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Margaret F Bedillion, Catherine F Moore, Elise M Weerts, Caroline A Arout, Hannah M Harris, Margaret Haney
{"title":"Pharmacotherapy for Cannabis Use Disorder: Preclinical and Clinical Models.","authors":"Margaret F Bedillion, Catherine F Moore, Elise M Weerts, Caroline A Arout, Hannah M Harris, Margaret Haney","doi":"10.1007/7854_2025_598","DOIUrl":"https://doi.org/10.1007/7854_2025_598","url":null,"abstract":"<p><p>Cannabis use disorder (CUD) is increasingly prevalent, and there are no FDA-approved medications to facilitate its treatment. Research on the development of CUD pharmacotherapies lags compared to other substance use disorders (SUDs), partly due to the difficulty in establishing robust preclinical models of cannabinoid self-administration. This chapter evaluates the translational pipeline, from preclinical and human laboratory models to randomized controlled clinical trials for CUD, reviewing medication effects observed within these models and discussing the challenges in translating preclinical and human laboratory findings, particularly regarding efficacy endpoints (e.g., prolonged abstinence versus a reduction in use). The chapter concludes by addressing future directions for improving translational validity and optimizing therapeutic development for CUD.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}