Current topics in behavioral neurosciences最新文献

{"title":"Insights into Overlapping Brain Networks for Anxiety and Alcohol Use Disorders.","authors":"Nicole L Zabik, Jennifer Urbano Blackford","doi":"10.1007/7854_2025_592","DOIUrl":"10.1007/7854_2025_592","url":null,"abstract":"<p><p>Alcohol use disorder (AUD) is a debilitating condition affecting over 30 million Americans. AUD commonly co-occurs with other disorders, like other substance use disorders, trauma-related disorders, and anxiety disorders. Of the numerous co-occurring disorders, anxiety disorders are the most pervasive: anxiety disorders serve as a risk factor for developing AUD, emerge as co-occurring disorders that maintain alcohol drinking, and impede the effectiveness of treatments for AUD. Anxiety, therefore, shapes the development, course, and treatment of AUDs. AUDs can also increase anxiety, suggesting a complex, bidirectional relation between alcohol use and anxiety. The intersection of AUDs and anxiety is also supported by their overlapping neural circuits, specifically neural circuits involved in stress responding, reward processing, and cognitive control. The current review highlights findings from several decades of research on how anxiety impacts the brain and treatment outcomes in AUDs. We also provide important considerations for future research, with the goal of reducing the shame and burden of alcohol use for individuals with AUD and their families.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"609-635"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12353971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143973607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Dopamine System in Mediating Alcohol Effects in Humans.","authors":"Anne Beck, Claudia Ebrahimi, Annika Rosenthal, Katrin Charlet, Andreas Heinz","doi":"10.1007/7854_2022_415","DOIUrl":"10.1007/7854_2022_415","url":null,"abstract":"<p><p>Brain-imaging studies show that the development and maintenance of alcohol use disorder (AUD) is determined by a complex interaction of different neurotransmitter systems and multiple psychological factors. In this context, the dopaminergic reinforcement system appears to be of fundamental importance. We focus on the excitatory and depressant effects of acute versus chronic alcohol intake and its impact on dopaminergic neurotransmission. Furthermore, we describe alterations in dopaminergic neurotransmission as associated with symptoms of alcohol dependence. We specifically focus on neuroadaptations to chronic alcohol consumption and their effect on central processing of alcohol-associated and reward-related stimuli. Altered reward processing, complex conditioning processes, impaired reinforcement learning, and increased salience attribution to alcohol-associated stimuli enable alcohol cues to drive alcohol seeking and consumption. Finally, we will discuss how the neurobiological and neurochemical mechanisms of alcohol-associated alterations in reward processing and learning can interact with stress, cognition, and emotion processing.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"475-518"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10623713","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":"Modulation of Alcohol Use Disorder by Brain Stimulation.","authors":"Noam Ygael, Abraham Zangen","doi":"10.1007/7854_2024_487","DOIUrl":"10.1007/7854_2024_487","url":null,"abstract":"<p><p>Currently available therapeutic modalities for alcohol use disorder (AUD) produce limited effect sizes or long-term compliance. Recent methods that were developed to modulate brain activity represent potential novel treatment options. Various methods of brain stimulation, when applied repeatedly, can induce long-term neurobiological, behavioral, and cognitive modifications. Recent studies in alcoholic subjects indicate the potential of brain stimulation methods to reduce alcohol craving, consumption, and relapse. Specifically, deep brain stimulation (DBS) of the nucleus accumbens or non-surgical stimulation of the dorsolateral prefrontal cortex (PFC) or medial PFC and anterior cingulate cortex using transcranial magnetic stimulation (TMS) has shown clinical benefit. However, further preclinical and clinical research is needed to establish understanding of mechanisms and the treatment protocols of brain stimulation for AUD. While efforts to design comparable apparatus in rodents continue, preclinical studies can be used to examine targets for DBS protocols, or to administer temporal patterns of pulsus similar to those used for TMS, to more superficial targets through implanted electrodes. The clinical field will benefit from studies with larger sample sizes, higher numbers of stimulation sessions, maintenance sessions, and long follow-up periods. The effect of symptoms provocation before and during stimulation should be further studied. Larger studies may have the power to explore predictive factors for the clinical outcome and thereby to optimize patient selection and eventually even develop personalization of the stimulation parameters.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"719-736"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141747724","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":"Molecular Imaging Studies of Alcohol Use Disorder.","authors":"Patrick Bach, Philippe de Timary, Gerhard Gründer, Paul Cumming","doi":"10.1007/7854_2022_414","DOIUrl":"10.1007/7854_2022_414","url":null,"abstract":"<p><p>Alcohol use disorder (AUD) is a serious public health problem in many countries, bringing a gamut of health risks and impairments to individuals and a great burden to society. Despite the prevalence of a disease model of AUD, the current pharmacopeia does not present reliable treatments for AUD; approved treatments are confined to a narrow spectrum of medications engaging inhibitory γ-aminobutyric acid (GABA) neurotransmission and possibly excitatory N-methyl-D-aspartate (NMDA) receptors, and opioid receptor antagonists. Molecular imaging with positron emission tomography (PET) and single-photon emission computed tomography (SPECT) can open a window into the living brain and has provided diverse insights into the pathology of AUD. In this narrative review, we summarize the state of molecular imaging findings on the pharmacological action of ethanol and the neuropathological changes associated with AUD. Laboratory and preclinical imaging results highlight the interactions between ethanol and GABA A-type receptors (GABA_AR), but the interpretation of such results is complicated by subtype specificity. An abundance of studies with the glucose metabolism tracer fluorodeoxyglucose (FDG) concur in showing cerebral hypometabolism after ethanol challenge, but there is relatively little data on long-term changes in AUD. Alcohol toxicity evokes neuroinflammation, which can be tracked using PET with ligands for the microglial marker translocator protein (TSPO). Several PET studies show reversible increases in TSPO binding in AUD individuals, and preclinical results suggest that opioid-antagonists can rescue from these inflammatory responses. There are numerous PET/SPECT studies showing changes in dopaminergic markers, generally consistent with an impairment in dopamine synthesis and release among AUD patients, as seen in a number of other addictions; this may reflect the composite of an underlying deficiency in reward mechanisms that predisposes to AUD, in conjunction with acquired alterations in dopamine signaling. There is little evidence for altered serotonin markers in AUD, but studies with opioid receptor ligands suggest a specific up-regulation of the μ-opioid receptor subtype. Considerable heterogeneity in drinking patterns, gender differences, and the variable contributions of genetics and pre-existing vulnerability traits present great challenges for charting the landscape of molecular imaging in AUD.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"519-549"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9090209","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":"New Approaches for Alcohol Use Disorder Treatment via Memory Retrieval and Reconsolidation Manipulations.","authors":"Segev Barak, Koral Goltseker","doi":"10.1007/7854_2022_411","DOIUrl":"10.1007/7854_2022_411","url":null,"abstract":"<p><p>Relapse to alcohol seeking and drinking is a major clinical challenge in alcohol use disorder and is frequently brought about by cue-induced craving, caused by exposure to cues that evoke alcohol-related memories. It has been postulated that memories become labile for manipulation shortly after their retrieval and then restabilize in a \"memory reconsolidation\" process. Disruption or interference with the reconsolidation of drug-associated memories has been suggested as a possible strategy to reduce or even prevent cue-induced craving and relapse. Here, we review literature demonstrating the capacity of behavioral or pharmacological manipulations to reduce relapse in animal models and humans when applied after a short retrieval of memories associated with alcohol, suggestively disrupting the reconsolidation of such memories. We suggest that while there is a clear potential of using post-retrieval manipulations to target specific relapse-evoking memories, future research should be more systematic, standardized, and translational. Specifically, we discuss several critical limitations and boundary conditions, which should be addressed to improve consistency and replicability in the field and lead to the development of an efficient reconsolidation-based relapse prevention therapy.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"621-639"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10569799","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":"Synaptic Effects Induced by Alcohol.","authors":"David M Lovinger, Marisa Roberto","doi":"10.1007/7854_2022_412","DOIUrl":"10.1007/7854_2022_412","url":null,"abstract":"<p><p>Ethanol (EtOH) has effects on numerous cellular molecular targets, and alterations in synaptic function are prominent among these effects. Acute exposure to EtOH activates or inhibits the function of proteins involved in synaptic transmission, while chronic exposure often produces opposing and/or compensatory/homeostatic effects on the expression, localization, and function of these proteins. Interactions between different neurotransmitters (e.g., neuropeptide effects on release of small molecule transmitters) can also influence both acute and chronic EtOH actions. Studies in intact animals indicate that the proteins affected by EtOH also play roles in the neural actions of the drug, including acute intoxication, tolerance, dependence, and the seeking and drinking of EtOH. The present chapter is an update of our previous Lovinger and Roberto (Curr Top Behav Neurosci 13:31-86, 2013) chapter and reviews the literature describing these acute and chronic synaptic effects of EtOH with a focus on adult animals and their relevance for synaptic transmission, plasticity, and behavior.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"217-308"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11104446/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10680172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholinergic System Structure and Function Changes in Individuals with Down Syndrome During the Development of Alzheimer's Disease.","authors":"Jason K Russell, Alexander C Conley, Jo Ellen Wilson, Paul A Newhouse","doi":"10.1007/7854_2024_523","DOIUrl":"10.1007/7854_2024_523","url":null,"abstract":"<p><p>Adults with Down syndrome represent the population with the highest risk of developing Alzheimer's disease worldwide. The cholinergic system is known to decline in Alzheimer's disease, with this decline responsible for many of the cognitive deficits that develop. The integrity of the cholinergic system across the lifespan in individuals with Down syndrome is not well characterized. Small fetal and infant post-mortem studies suggest an intact cholinergic projection system with a potential reduction in cholinergic receptors, while post-mortem studies in adults with Down syndrome reveal an age-related decrease in cholinergic integrity. Advances in magnetic resonance imaging (MRI) and positron emission tomography (PET) over the last 20 years have allowed for studies investigating the changes in cholinergic integrity across aging and during the development of Alzheimer's disease. One large cross-sectional study demonstrated reduced cholinergic basal forebrain volume measured by MRI associated with increasing Alzheimer's disease pathology. In a small cohort of adults with Down syndrome, we have recently reported that PET measures of cholinergic integrity negatively correlated with amyloid accumulation. New disease-modifying treatments for Alzheimer's disease and treatments under development for Alzheimer's disease in Down syndrome have the potential to preserve the cholinergic system, while treatments targeting the cholinergic system directly may be used in conjunction with disease-modifying therapies to improve cognitive function further. A greater understanding of cholinergic neuronal and receptor integrity across the lifespan in individuals with Down syndrome will provide insights as to when targeting the cholinergic system is an appropriate therapeutic option and, in the future, maybe a valuable screening tool to identify individuals that would most benefit from cholinergic interventions.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"49-78"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12042956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142562401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental Shifts in Amygdala Function.","authors":"J Amiel Rosenkranz","doi":"10.1007/7854_2024_538","DOIUrl":"10.1007/7854_2024_538","url":null,"abstract":"<p><p>Mammals have evolved with strategies to optimize survival and thrive in their native environment. This includes both physical and behavioral adaptations, and extends to their social environment. However, within a social context, the roles of an animal change across development, and their behavior and biology must update to match these changes. The amygdala has a key role in social and emotional processing and expression, and displays developmental changes in early juvenile, adolescent, and adult transitions. Furthermore, the amygdala is highly sensitive to the social environment. This chapter will describe the primary amygdala developmental changes, how this maps onto major changes in social and emotional domains, and propose a framework where developmental stage of intra-amygdala circuits and its regulation by cortical inputs biases the animal toward developmentally appropriate social and emotional behavior. This developmental plasticity also presents an opportunity for retuning the developmental trajectory in the presence of ongoing challenges during maturation, such as constant threat or resource scarcity, so there can be realignment of behavior to match environmental demands.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"207-229"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12107673/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142638232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural Brain Correlates of Anxiety During Development.","authors":"E Leighton Durham, Antonia N Kaczkurkin","doi":"10.1007/7854_2024_541","DOIUrl":"10.1007/7854_2024_541","url":null,"abstract":"<p><p>Anxiety and related disorders are prevalent across the lifespan, often have their onset during youth, and are associated with notable levels of impairment and burden across multiple domains. Elucidating the associations between differential patterns of neurodevelopment and anxiety in youth is a promising approach for developing deeper insights regarding the neurobiological etiologies and maintenance factors associated with anxiety and related disorders. A growing body of literature has yielded evidence of associations between patterns of brain structure (i.e., volume, cortical thickness, and cortical surface area) and anxiety. Here, we present a review and synthesis of the existing body of literature surrounding neurostructural correlates of anxiety in youth spanning multiple anxiety presentations and three neurostructural modalities. We reveal substantially more research focusing on brain volume than cortical thickness or surface area and a greater number of studies examining anxiety broadly defined, obsessive-compulsive disorder, or posttraumatic stress disorder. There is also evidence of considerable variability in the brain regions implicated and the direction of associations across studies. Finally, we discuss the gaps and limitations in this body of work, which suggest avenues for future directions.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"123-153"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603363","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":"Insights into the Neurobiology of Behavioral Inhibition from Nonhuman Primate Models.","authors":"Lillian J Campos, Carly M Drzewiecki, Andrew S Fox","doi":"10.1007/7854_2024_561","DOIUrl":"10.1007/7854_2024_561","url":null,"abstract":"<p><p>Children with extreme behavioral inhibition (BI) are at a significantly greater risk to develop anxiety disorders later in life. We and others have identified similar early-life temperamental BI in nonhuman primates (NHPs), including rhesus monkeys. NHP models of BI provide a unique opportunity to study the neurobiology of BI in a species that shares biological, developmental, and socioemotional similarities with humans. Rhesus monkey models have identified a distributed brain circuit that includes the central extended amygdala (EAc) as being critical for the genesis of BI. By leveraging multimodal neuroimaging, brain lesions, RNA-sequencing, and viral vector manipulations in rhesus monkeys, these studies have identified specific brain regions, genetic factors, and molecular mechanisms that causally contribute to BI. Here, we discuss these findings from NHPs and how they fit into a translational framework that can contribute to our understanding of the neural circuits that give rise to the risk to develop anxiety and depressive disorders.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"253-275"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909593","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}