Avoidance behaviors are paramount for the survival of all species. While adaptive in response to genuine danger, avoidance can become maladaptive when generalized or persistent in the absence of threat. In anxiety disorders, maladaptive avoidance behaviors frequently arise and impede everyday life for individuals with these mental health conditions. Given the central role of avoidance in anxiety disorders, understanding the neural circuits that underly these behaviors is essential for developing both targeted and effective treatments. This review explores avoidance through both a behavioral and neural mechanistic lens, while also examining the current behavioral and pharmacological treatments aimed at addressing avoidance. Understanding of the neural underpinnings of avoidance, psychotherapy, and pharmacotherapy may improve clinical care and outcomes for those suffering with anxiety disorders.
{"title":"Behavioral and Brain Mechanisms of Active Avoidance and Their Relevance to Anxiety Disorders.","authors":"Hannah McManus, Mohammed R Milad","doi":"10.1007/7854_2025_593","DOIUrl":"10.1007/7854_2025_593","url":null,"abstract":"<p><p>Avoidance behaviors are paramount for the survival of all species. While adaptive in response to genuine danger, avoidance can become maladaptive when generalized or persistent in the absence of threat. In anxiety disorders, maladaptive avoidance behaviors frequently arise and impede everyday life for individuals with these mental health conditions. Given the central role of avoidance in anxiety disorders, understanding the neural circuits that underly these behaviors is essential for developing both targeted and effective treatments. This review explores avoidance through both a behavioral and neural mechanistic lens, while also examining the current behavioral and pharmacological treatments aimed at addressing avoidance. Understanding of the neural underpinnings of avoidance, psychotherapy, and pharmacotherapy may improve clinical care and outcomes for those suffering with anxiety disorders.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"57-72"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144265606","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}
Pub Date : 2025-01-01DOI: 10.1007/978-3-031-84920-6_577
Arianna Di Stadio, Mickie J Hamiter, Dalila Roccamatisi, Anil K Lalwani
{"title":"Correction to: Hearing Loss and Alzheimer Disease.","authors":"Arianna Di Stadio, Mickie J Hamiter, Dalila Roccamatisi, Anil K Lalwani","doi":"10.1007/978-3-031-84920-6_577","DOIUrl":"https://doi.org/10.1007/978-3-031-84920-6_577","url":null,"abstract":"","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":"69 ","pages":"C3"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069270","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}
Humans consume ethanol-containing beverages, which may cause an uncontrollable or difficult-to-control intake of ethanol-containing liquids and may result in alcohol use disorders. How the transition at the molecular level from "normal" ethanol-associated behaviors to addictive behaviors occurs is still unknown. One problem is that the components contributing to normal ethanol intake and their underlying molecular adaptations, especially in neurons that regulate behavior, are not clear. The fruit fly Drosophila melanogaster and the earthworm Caenorhabditis elegans show behavioral similarities to humans such as signs of intoxication, tolerance, and withdrawal. Underlying the phenotypic similarities, invertebrates and vertebrates share mechanistic similarities. For example in Drosophila melanogaster, the dopaminergic neurotransmitter system regulates the positive reinforcing properties of ethanol and in Caenorhabditis elegans, serotonergic neurons regulate feeding behavior. Since these mechanisms are fundamental molecular mechanisms and are highly conserved, invertebrates are good models for uncovering the basic principles of neuronal adaptation underlying the behavioral response to ethanol. This review will focus on the following aspects that might shed light on the mechanisms underlying normal ethanol-associated behaviors. First, the current status of what is required at the behavioral and cellular level to respond to naturally occurring levels of ethanol is summarized. Low levels of ethanol delay the development and activate compensatory mechanisms that in turn might be beneficial for some aspects of the animal's physiology. Repeated exposure to ethanol however might change brain structures involved in mediating learning and memory processes. The smell of ethanol is already a key component in the environment that is able to elicit behavioral changes and molecular programs. Minimal networks have been identified that regulate normal ethanol consumption. Other environmental factors that influence ethanol-induced behaviors include the diet, dietary supplements, and the microbiome. Second, the molecular mechanisms underlying neuronal adaptation to the cellular stressor ethanol are discussed. Components of the heat shock and oxidative stress pathways regulate adaptive responses to low levels of ethanol and in turn change behavior. The adaptive potential of the brain cells is challenged when the organism encounters additional cellular stressors caused by aging, endosymbionts or environmental toxins or excessive ethanol intake. Finally, to underline the conserved nature of these mechanisms between invertebrates and higher organisms, recent approaches to identify drug targets for ethanol-induced behaviors are provided. Already approved drugs regulate ethanol-induced behaviors and they do so in part by interfering with cellular stress pathways. In addition, invertebrates have been used to identify new compounds targeting molecules involved in the re
{"title":"From Natural Behavior to Drug Screening: Invertebrates as Models to Study Mechanisms Associated with Alcohol Use Disorders.","authors":"Henrike Scholz","doi":"10.1007/7854_2022_413","DOIUrl":"10.1007/7854_2022_413","url":null,"abstract":"<p><p>Humans consume ethanol-containing beverages, which may cause an uncontrollable or difficult-to-control intake of ethanol-containing liquids and may result in alcohol use disorders. How the transition at the molecular level from \"normal\" ethanol-associated behaviors to addictive behaviors occurs is still unknown. One problem is that the components contributing to normal ethanol intake and their underlying molecular adaptations, especially in neurons that regulate behavior, are not clear. The fruit fly Drosophila melanogaster and the earthworm Caenorhabditis elegans show behavioral similarities to humans such as signs of intoxication, tolerance, and withdrawal. Underlying the phenotypic similarities, invertebrates and vertebrates share mechanistic similarities. For example in Drosophila melanogaster, the dopaminergic neurotransmitter system regulates the positive reinforcing properties of ethanol and in Caenorhabditis elegans, serotonergic neurons regulate feeding behavior. Since these mechanisms are fundamental molecular mechanisms and are highly conserved, invertebrates are good models for uncovering the basic principles of neuronal adaptation underlying the behavioral response to ethanol. This review will focus on the following aspects that might shed light on the mechanisms underlying normal ethanol-associated behaviors. First, the current status of what is required at the behavioral and cellular level to respond to naturally occurring levels of ethanol is summarized. Low levels of ethanol delay the development and activate compensatory mechanisms that in turn might be beneficial for some aspects of the animal's physiology. Repeated exposure to ethanol however might change brain structures involved in mediating learning and memory processes. The smell of ethanol is already a key component in the environment that is able to elicit behavioral changes and molecular programs. Minimal networks have been identified that regulate normal ethanol consumption. Other environmental factors that influence ethanol-induced behaviors include the diet, dietary supplements, and the microbiome. Second, the molecular mechanisms underlying neuronal adaptation to the cellular stressor ethanol are discussed. Components of the heat shock and oxidative stress pathways regulate adaptive responses to low levels of ethanol and in turn change behavior. The adaptive potential of the brain cells is challenged when the organism encounters additional cellular stressors caused by aging, endosymbionts or environmental toxins or excessive ethanol intake. Finally, to underline the conserved nature of these mechanisms between invertebrates and higher organisms, recent approaches to identify drug targets for ethanol-induced behaviors are provided. Already approved drugs regulate ethanol-induced behaviors and they do so in part by interfering with cellular stress pathways. In addition, invertebrates have been used to identify new compounds targeting molecules involved in the re","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"145-167"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10826796","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}
Alcohol use disorder (AUD) induces significant structural alterations in both gray and white matter, contributing to cognitive and functional impairments. This chapter presents a translational neuroimaging approach using diffusion-weighted MRI in humans and rodents to uncover novel pathophysiological mechanisms underlying AUD. Our studies demonstrate that increased mean diffusivity (MD) in gray matter reflects microglial reactivity and reduced extracellular space tortuosity, leading to enhanced volume neurotransmission. In white matter, fractional anisotropy (FA) reductions indicate progressive deterioration of key tracts, particularly the fimbria/fornix, linked to impaired cognitive flexibility. Importantly, longitudinal analyses reveal that white matter degeneration continues during early abstinence, suggesting that neuroinflammation and demyelination persist beyond alcohol cessation. Finally, we discuss how neuromodulatory interventions, such as transcranial magnetic stimulation (TMS), may promote recovery by enhancing myelin plasticity. These findings provide crucial insights into AUD's neurobiological underpinnings and highlight potential therapeutic targets for improving treatment outcomes.
{"title":"Alcohol-Induced Changes in Brain Microstructure: Uncovering Novel Pathophysiological Mechanisms of AUD Using Translational DTI in Humans and Rodents.","authors":"Wolfgang H Sommer, Santiago Canals","doi":"10.1007/7854_2025_585","DOIUrl":"10.1007/7854_2025_585","url":null,"abstract":"<p><p>Alcohol use disorder (AUD) induces significant structural alterations in both gray and white matter, contributing to cognitive and functional impairments. This chapter presents a translational neuroimaging approach using diffusion-weighted MRI in humans and rodents to uncover novel pathophysiological mechanisms underlying AUD. Our studies demonstrate that increased mean diffusivity (MD) in gray matter reflects microglial reactivity and reduced extracellular space tortuosity, leading to enhanced volume neurotransmission. In white matter, fractional anisotropy (FA) reductions indicate progressive deterioration of key tracts, particularly the fimbria/fornix, linked to impaired cognitive flexibility. Importantly, longitudinal analyses reveal that white matter degeneration continues during early abstinence, suggesting that neuroinflammation and demyelination persist beyond alcohol cessation. Finally, we discuss how neuromodulatory interventions, such as transcranial magnetic stimulation (TMS), may promote recovery by enhancing myelin plasticity. These findings provide crucial insights into AUD's neurobiological underpinnings and highlight potential therapeutic targets for improving treatment outcomes.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"595-617"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990809","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}
Jecenia Duran, Sonia Khalid, Lauren Richardson, Kelly Bosse, Susanne Brummelte
Opioid use disorder (OUD) continues to be a global problem, with particularly high opioid usage rates in the United States. One major contributor to this crisis has been the high rate of opioid prescriptions, which has increased access to opioids and contributed to many vulnerable individuals becoming dependent or addicted. Many of these affected people are women of reproductive age, which in turn results in many women using or abusing opioids during pregnancy and thus many infants being exposed to illicit opioids. OUD is typically treated with either methadone or buprenorphine (BUP), two effective opioid-based medications for OUD (MOUD). BUP has recently gained more attention and replaced methadone as the "gold standard" of treatment since its unique pharmacodynamic properties seem to result in better compliance, less withdrawal symptoms, and improved infant outcomes compared to methadone. However, the effects of BUP exposure on the long-term outcome of the offspring and mother-infant dyad are not fully understood. This chapter will review the current state of the literature regarding effects of gestational opioid exposure on offspring outcomes, focusing on morphine as a commonly used illicit substance and BUP as a widely used MOUD. Collectively, the literature reviewed here highlights the need for future research into the impact of gestational opioid use on mothers, their care behavior, and their subsequent mother-infant bonds.
{"title":"Gestational Opioid Exposure: From Morphine to MOUD - How Opioids Impact Offspring Development and Maternal Care.","authors":"Jecenia Duran, Sonia Khalid, Lauren Richardson, Kelly Bosse, Susanne Brummelte","doi":"10.1007/7854_2024_570","DOIUrl":"10.1007/7854_2024_570","url":null,"abstract":"<p><p>Opioid use disorder (OUD) continues to be a global problem, with particularly high opioid usage rates in the United States. One major contributor to this crisis has been the high rate of opioid prescriptions, which has increased access to opioids and contributed to many vulnerable individuals becoming dependent or addicted. Many of these affected people are women of reproductive age, which in turn results in many women using or abusing opioids during pregnancy and thus many infants being exposed to illicit opioids. OUD is typically treated with either methadone or buprenorphine (BUP), two effective opioid-based medications for OUD (MOUD). BUP has recently gained more attention and replaced methadone as the \"gold standard\" of treatment since its unique pharmacodynamic properties seem to result in better compliance, less withdrawal symptoms, and improved infant outcomes compared to methadone. However, the effects of BUP exposure on the long-term outcome of the offspring and mother-infant dyad are not fully understood. This chapter will review the current state of the literature regarding effects of gestational opioid exposure on offspring outcomes, focusing on morphine as a commonly used illicit substance and BUP as a widely used MOUD. Collectively, the literature reviewed here highlights the need for future research into the impact of gestational opioid use on mothers, their care behavior, and their subsequent mother-infant bonds.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"149-182"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604288","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}
Early indicators of anxiety risk can appear as early as infancy, informing developmental pathways in which individual differences in temperament elevate the likelihood of future anxiety disorders. Clarifying the mechanisms that connect these early biological predispositions to later anxiety offers a foundation for designing targeted early intervention and prevention efforts. In this chapter, we aim to describe the association between fearful temperament and the development of anxiety disorders, highlighting how the interplay between biological and environmental factors shape vulnerability to anxiety from early in life. We describe (a) fearful temperament as a potential marker for vulnerability to anxiety, (b) neural mechanisms underlying fearful temperament and anxiety through detection and regulation processes, (c) internal and external factors that moderate the association between fearful temperament and anxiety, focusing on attentional bias and parental factors to understand distinct etiological process.
{"title":"Neurodevelopmental Pathways from Temperamental Fear to Anxiety.","authors":"Eunkyung Shin, Koraly Pérez-Edgar","doi":"10.1007/7854_2024_571","DOIUrl":"10.1007/7854_2024_571","url":null,"abstract":"<p><p>Early indicators of anxiety risk can appear as early as infancy, informing developmental pathways in which individual differences in temperament elevate the likelihood of future anxiety disorders. Clarifying the mechanisms that connect these early biological predispositions to later anxiety offers a foundation for designing targeted early intervention and prevention efforts. In this chapter, we aim to describe the association between fearful temperament and the development of anxiety disorders, highlighting how the interplay between biological and environmental factors shape vulnerability to anxiety from early in life. We describe (a) fearful temperament as a potential marker for vulnerability to anxiety, (b) neural mechanisms underlying fearful temperament and anxiety through detection and regulation processes, (c) internal and external factors that moderate the association between fearful temperament and anxiety, focusing on attentional bias and parental factors to understand distinct etiological process.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"329-353"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604290","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}
Participant recruitment and retention into randomized controlled trials (RCTs) is a growing and evolving science. It varies dramatically by discipline given the important and key choices that must be made based on the unique trial design considerations. In the field of Alzheimer's Disease (AD) therapeutics, recruitment goals, approaches, and strategies vary based on the disease stage of the target population which can range from asymptomatic adults with biomarker evidence of the disease to end-stage symptom management. This chapter discusses existing barriers and provides recommendations to achieve inclusive and timely recruitment in multi-center AD trials. It proposes an evidence-based recruitment framework anchored on culturally cognizant and participant focused study level and study site level efforts.
{"title":"Achieving Inclusion in Pharmacological Clinical Trials for Alzheimer's Disease.","authors":"Doris Molina-Henry, Rema Raman","doi":"10.1007/7854_2024_522","DOIUrl":"10.1007/7854_2024_522","url":null,"abstract":"<p><p>Participant recruitment and retention into randomized controlled trials (RCTs) is a growing and evolving science. It varies dramatically by discipline given the important and key choices that must be made based on the unique trial design considerations. In the field of Alzheimer's Disease (AD) therapeutics, recruitment goals, approaches, and strategies vary based on the disease stage of the target population which can range from asymptomatic adults with biomarker evidence of the disease to end-stage symptom management. This chapter discusses existing barriers and provides recommendations to achieve inclusive and timely recruitment in multi-center AD trials. It proposes an evidence-based recruitment framework anchored on culturally cognizant and participant focused study level and study site level efforts.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"229-242"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142817629","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}
Most anxiety disorders 'run within families': people suffering from an anxiety disorder often have family members who are highly anxious as well. In this chapter, we explore recent work devoted to unraveling the complex interplay between genes and environment in the development of anxiety. We review studies focusing on the genetic vulnerability to develop social anxiety disorder (SAD), as SAD is one of the most prevalent anxiety disorders, with an early onset, a chronic course, and associated with significant life-long impairments. More insight into the development of SAD is thus of uttermost importance.First, we will discuss family studies, twin studies, and large-sized population-based registry studies and explain what these studies can reveal about the genetic vulnerability to develop anxiety. Next, we describe the endophenotype approach; in this context, we will summarize results from the Leiden Family Lab study on Social Anxiety Disorder. Subsequently, we review the relationship between the heritable trait 'behavioral inhibition' and the development of SAD, and highlight the relevance of this work for the development and improvement of preventative and therapeutic interventions for socially anxious youth.
{"title":"Genetic Vulnerability to Social Anxiety Disorder.","authors":"Janna Marie Bas-Hoogendam","doi":"10.1007/7854_2024_544","DOIUrl":"10.1007/7854_2024_544","url":null,"abstract":"<p><p>Most anxiety disorders 'run within families': people suffering from an anxiety disorder often have family members who are highly anxious as well. In this chapter, we explore recent work devoted to unraveling the complex interplay between genes and environment in the development of anxiety. We review studies focusing on the genetic vulnerability to develop social anxiety disorder (SAD), as SAD is one of the most prevalent anxiety disorders, with an early onset, a chronic course, and associated with significant life-long impairments. More insight into the development of SAD is thus of uttermost importance.First, we will discuss family studies, twin studies, and large-sized population-based registry studies and explain what these studies can reveal about the genetic vulnerability to develop anxiety. Next, we describe the endophenotype approach; in this context, we will summarize results from the Leiden Family Lab study on Social Anxiety Disorder. Subsequently, we review the relationship between the heritable trait 'behavioral inhibition' and the development of SAD, and highlight the relevance of this work for the development and improvement of preventative and therapeutic interventions for socially anxious youth.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"301-328"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616618","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}
Performing and perceiving music requires the integration of multimodal information, including sensations of one's own body. Research on musical engagement investigated emotional responses and the peripheral physiological activations involved, as well as bodily action tendencies, effects on time perception, and the role of awareness and focus of attention. The concept of interoception dedicates a central role to the insular cortex, as suggested by Craig and others, and offers a unifying framework for studying music as an activity that has always had a key role for individuals, groups, societies, with a strong bodily component. Chances and challenges of an interoceptive perspective on music are discussed.
{"title":"Music in the Air and in the Body: An Interoceptive System's Perspective on Musical Emotions, Awareness, and Time.","authors":"Clemens Wöllner","doi":"10.1007/7854_2024_517","DOIUrl":"10.1007/7854_2024_517","url":null,"abstract":"<p><p>Performing and perceiving music requires the integration of multimodal information, including sensations of one's own body. Research on musical engagement investigated emotional responses and the peripheral physiological activations involved, as well as bodily action tendencies, effects on time perception, and the role of awareness and focus of attention. The concept of interoception dedicates a central role to the insular cortex, as suggested by Craig and others, and offers a unifying framework for studying music as an activity that has always had a key role for individuals, groups, societies, with a strong bodily component. Chances and challenges of an interoceptive perspective on music are discussed.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"269-284"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142460395","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}
The mind is embodied, and this is relevant to mental health and psychiatric illness. Interoception is the body-to-brain axis of sensory information flow and its representation at the neural and psychological levels. Interoception is the purported basis for motivation and emotion, and as an inescapable stream of information about the health and functioning of the whole organism, it is proposed to be the foundation to the conscious unitary sense of self. Correspondingly, this central representation of internal state is relevant to understanding the expression of psychological symptoms and behaviours and ultimately psychiatric disorders. Here we review interoception, particularly from a cardiovascular perspective, and how understanding theoretical neural and psychological aspects of interoception relates to perceptions, thoughts, and feelings. We examine how perturbations in interoceptive processing are expressed in mental symptoms and psychiatric disorders and show how this knowledge may yield new treatment targets.
{"title":"Interoception, Insula, and Autonomic Integration: Relevance to the Expression and Treatment of Psychiatric Symptoms.","authors":"Hugo D Critchley, Joel Patchitt","doi":"10.1007/7854_2024_518","DOIUrl":"10.1007/7854_2024_518","url":null,"abstract":"<p><p>The mind is embodied, and this is relevant to mental health and psychiatric illness. Interoception is the body-to-brain axis of sensory information flow and its representation at the neural and psychological levels. Interoception is the purported basis for motivation and emotion, and as an inescapable stream of information about the health and functioning of the whole organism, it is proposed to be the foundation to the conscious unitary sense of self. Correspondingly, this central representation of internal state is relevant to understanding the expression of psychological symptoms and behaviours and ultimately psychiatric disorders. Here we review interoception, particularly from a cardiovascular perspective, and how understanding theoretical neural and psychological aspects of interoception relates to perceptions, thoughts, and feelings. We examine how perturbations in interoceptive processing are expressed in mental symptoms and psychiatric disorders and show how this knowledge may yield new treatment targets.</p>","PeriodicalId":11257,"journal":{"name":"Current topics in behavioral neurosciences","volume":" ","pages":"63-85"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142616623","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}