Pub Date : 2025-08-14DOI: 10.1016/j.conb.2025.103094
Gabriel J. Graham, Justin S. Rhodes
Sex determination in coral reef fish is highly plastic, with many species displaying socially controlled sequential hermaphroditism. In these species, social hierarchy cues trigger sex change, initiating transformations in neuroanatomy, physiology, morphology, and behavior. The process begins in the brain, where shifts in dominance status alter cortisol release and neuromodulator signaling, including dopamine and arginine vasotocin. Radial glia detect these changes and modulate local estradiol synthesis via brain aromatase production that in turn influences neurogenesis and gene expression in multiple types of glia and neurons involved in pituitary-gonadotroph regulation. The altered gonadotroph control directs the gonadal transformation. Mechanistically, protogyny (female-to-male) typically occurs faster than protandry (male-to-female), with differences in the order of behavioral, gonadal, and morphological changes. Understanding these processes in sex-changing fish provides valuable insights into the neural and endocrine mechanisms underlying reproductive plasticity, with broader implications for neuroendocrinology and the evolution of sex differences in vertebrates.
{"title":"Plasticity of brain sexual dimorphism as revealed by sex changing fish","authors":"Gabriel J. Graham, Justin S. Rhodes","doi":"10.1016/j.conb.2025.103094","DOIUrl":"10.1016/j.conb.2025.103094","url":null,"abstract":"<div><div>Sex determination in coral reef fish is highly plastic, with many species displaying socially controlled sequential hermaphroditism. In these species, social hierarchy cues trigger sex change, initiating transformations in neuroanatomy, physiology, morphology, and behavior. The process begins in the brain, where shifts in dominance status alter cortisol release and neuromodulator signaling, including dopamine and arginine vasotocin. Radial glia detect these changes and modulate local estradiol synthesis via brain aromatase production that in turn influences neurogenesis and gene expression in multiple types of glia and neurons involved in pituitary-gonadotroph regulation. The altered gonadotroph control directs the gonadal transformation. Mechanistically, protogyny (female-to-male) typically occurs faster than protandry (male-to-female), with differences in the order of behavioral, gonadal, and morphological changes. Understanding these processes in sex-changing fish provides valuable insights into the neural and endocrine mechanisms underlying reproductive plasticity, with broader implications for neuroendocrinology and the evolution of sex differences in vertebrates.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"94 ","pages":"Article 103094"},"PeriodicalIF":5.2,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144829435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Astrocytes emerge as pivotal regulators of brain plasticity during critical periods (CPs) of development. Beyond their traditional roles in supporting neuronal function, astrocytes actively shape synaptic circuits maturation and remodeling during postnatal experience-dependent plasticity. Through mechanisms such as regulation of the extracellular matrix or synaptic pruning, astrocytes influence the timing and extent of plasticity across sensory and cognitive systems. These processes have been demonstrated in various animal models and forms of plasticity, indicating that these glial cells play a conserved role across species. Such findings unveil the dynamic and central role of astrocytes in coordinating the complex interplay between neural circuits and external stimuli during critical windows of brain development.
{"title":"Astroglial regulation of critical period plasticity in the developing brain","authors":"Jérôme Ribot , Rachel Breton , Glenn Dallérac , Nathalie Rouach","doi":"10.1016/j.conb.2025.103092","DOIUrl":"10.1016/j.conb.2025.103092","url":null,"abstract":"<div><div>Astrocytes emerge as pivotal regulators of brain plasticity during critical periods (CPs) of development. Beyond their traditional roles in supporting neuronal function, astrocytes actively shape synaptic circuits maturation and remodeling during postnatal experience-dependent plasticity. Through mechanisms such as regulation of the extracellular matrix or synaptic pruning, astrocytes influence the timing and extent of plasticity across sensory and cognitive systems. These processes have been demonstrated in various animal models and forms of plasticity, indicating that these glial cells play a conserved role across species. Such findings unveil the dynamic and central role of astrocytes in coordinating the complex interplay between neural circuits and external stimuli during critical windows of brain development.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"94 ","pages":"Article 103092"},"PeriodicalIF":5.2,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144827805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-04-09DOI: 10.1016/j.conb.2025.103020
Aaron R. Seitz
Do we choose what we learn? On the contrary, research suggests that much of learning is incidental. The present article reviews frameworks of incidental statistical and perceptual learning and discusses implications of these frameworks to memory. This research supports the premise that much of what we know is shaped by statistical regularities in the environment, how our attention is directed, and what reinforcement we receive from successes and failures. This incidental learning shapes what we perceive and what we remember. This idea that we don’t control when and what we learn, instead we at best trick our brain into states that will lead to desired learning outcomes, has important implications both to individuals and society.
{"title":"Tricking our brains to learn and remember; is all learning incidental?","authors":"Aaron R. Seitz","doi":"10.1016/j.conb.2025.103020","DOIUrl":"10.1016/j.conb.2025.103020","url":null,"abstract":"<div><div>Do we choose what we learn? On the contrary, research suggests that much of learning is incidental. The present article reviews frameworks of incidental statistical and perceptual learning and discusses implications of these frameworks to memory. This research supports the premise that much of what we know is shaped by statistical regularities in the environment, how our attention is directed, and what reinforcement we receive from successes and failures. This incidental learning shapes what we perceive and what we remember. This idea that we don’t control when and what we learn, instead we at best trick our brain into states that will lead to desired learning outcomes, has important implications both to individuals and society.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103020"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143808619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-04-22DOI: 10.1016/j.conb.2025.103029
Benjamin J. Menarchek, Michelle C.D. Bridi
Sleep is thought to serve an important role in learning and memory, but the mechanisms by which sleep promotes plasticity remain unclear. Even in the absence of plastic changes in neuronal function, many molecular, cellular, and physiological processes linked to plasticity are upregulated during sleep. Therefore, sleep may be a state in which latent plasticity mechanisms are poised to respond following novel experiences during prior wake. Many of these plasticity-related processes can promote both synaptic strengthening and weakening. Signaling pathways activated during sleep may interact with complements of proteins, determined by the content of prior waking experience, to establish the polarity of plasticity. Furthermore, precise reactivation of neuronal spiking patterns during sleep may interact with ongoing neuromodulatory, dendritic, and network activity to strengthen and weaken synapses. In this review, we will discuss the idea that sleep elevates latent plasticity mechanisms, which drive bidirectional plasticity depending on prior waking experience.
{"title":"Latent mechanisms of plasticity are upregulated during sleep","authors":"Benjamin J. Menarchek, Michelle C.D. Bridi","doi":"10.1016/j.conb.2025.103029","DOIUrl":"10.1016/j.conb.2025.103029","url":null,"abstract":"<div><div>Sleep is thought to serve an important role in learning and memory, but the mechanisms by which sleep promotes plasticity remain unclear. Even in the absence of plastic changes in neuronal function, many molecular, cellular, and physiological processes linked to plasticity are upregulated during sleep. Therefore, sleep may be a state in which latent plasticity mechanisms are poised to respond following novel experiences during prior wake. Many of these plasticity-related processes can promote both synaptic strengthening and weakening. Signaling pathways activated during sleep may interact with complements of proteins, determined by the content of prior waking experience, to establish the polarity of plasticity. Furthermore, precise reactivation of neuronal spiking patterns during sleep may interact with ongoing neuromodulatory, dendritic, and network activity to strengthen and weaken synapses. In this review, we will discuss the idea that sleep elevates latent plasticity mechanisms, which drive bidirectional plasticity depending on prior waking experience.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103029"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143860335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-04-30DOI: 10.1016/j.conb.2025.103032
Kasey L. Brida, Jeremy J. Day
Drugs of abuse result in well-characterized changes in synapse function and number in brain reward regions such as the nucleus accumbens. However, recent reports demonstrate that only a small fraction of neurons in the nucleus accumbens are activated in response to psychostimulants such as cocaine. While these “ensemble” neurons are marked by drug-related transcriptional changes in immediate early genes, the mechanisms that ultimately link these early changes to enduring molecular alterations in the same neurons are less clear. In this review, we 1) describe potential mechanisms underlying regulation of diverse plasticity-related gene programs across drug-activated ensembles, 2) discuss factors conferring ensemble recruitment bias within seemingly homogeneous populations, and 3) speculate on the role of chromatin and epigenetic modifiers in gating metaplastic state transitions that contribute to addiction.
{"title":"Molecular and genetic mechanisms of plasticity in addiction","authors":"Kasey L. Brida, Jeremy J. Day","doi":"10.1016/j.conb.2025.103032","DOIUrl":"10.1016/j.conb.2025.103032","url":null,"abstract":"<div><div>Drugs of abuse result in well-characterized changes in synapse function and number in brain reward regions such as the nucleus accumbens. However, recent reports demonstrate that only a small fraction of neurons in the nucleus accumbens are activated in response to psychostimulants such as cocaine. While these “ensemble” neurons are marked by drug-related transcriptional changes in immediate early genes, the mechanisms that ultimately link these early changes to enduring molecular alterations in the same neurons are less clear. In this review, we 1) describe potential mechanisms underlying regulation of diverse plasticity-related gene programs across drug-activated ensembles, 2) discuss factors conferring ensemble recruitment bias within seemingly homogeneous populations, and 3) speculate on the role of chromatin and epigenetic modifiers in gating metaplastic state transitions that contribute to addiction.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103032"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143885948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-06-23DOI: 10.1016/j.conb.2025.103069
Inês C. Dias , Nicolas Gutierrez-Castellanos , Constanze Lenschow , Susana Q. Lima
Female sexual behavior is essential for reproduction and species survival. It is orchestrated by hormonal and neuronal mechanisms that coordinate sexual maturation, reproductive cycle, and the copulatory sequence, preparing the female for pregnancy. These mechanisms synchronize behavioral receptivity with reproductive capacity, ensuring that copulation occurs during optimal reproductive windows while actively suppressing sexual behavior outside fertile periods.
This review explores recent advances in neural mechanisms that integrate sensory, hormonal, and social cues in the female brain. We examine the main phases of sexual behavior: appetitive, consummatory, and refractory, focusing on the neural basis of sexual rejection during non-fertile periods. We also discuss studies using intersectional genetics and neural activity analysis to uncover the circuits underlying sexual receptivity and recent findings on how the female brain processes male ejaculation to trigger the refractory period. Altogether, this review sheds light on the orchestration of mating and reproductive readiness in female mice.
{"title":"Ready or not: Neural mechanisms regulating female sexual behavior","authors":"Inês C. Dias , Nicolas Gutierrez-Castellanos , Constanze Lenschow , Susana Q. Lima","doi":"10.1016/j.conb.2025.103069","DOIUrl":"10.1016/j.conb.2025.103069","url":null,"abstract":"<div><div>Female sexual behavior is essential for reproduction and species survival. It is orchestrated by hormonal and neuronal mechanisms that coordinate sexual maturation, reproductive cycle, and the copulatory sequence, preparing the female for pregnancy. These mechanisms synchronize behavioral receptivity with reproductive capacity, ensuring that copulation occurs during optimal reproductive windows while actively suppressing sexual behavior outside fertile periods.</div><div>This review explores recent advances in neural mechanisms that integrate sensory, hormonal, and social cues in the female brain. We examine the main phases of sexual behavior: appetitive, consummatory, and refractory, focusing on the neural basis of sexual rejection during non-fertile periods. We also discuss studies using intersectional genetics and neural activity analysis to uncover the circuits underlying sexual receptivity and recent findings on how the female brain processes male ejaculation to trigger the refractory period. Altogether, this review sheds light on the orchestration of mating and reproductive readiness in female mice.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103069"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144364951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-07-07DOI: 10.1016/j.conb.2025.103086
Madison T. Gray , Julie L. Lefebvre
Synaptic partner recognition and precise connectivity are essential components of neural circuit formation and function. Cell adhesion molecules with selective binding properties provide instructive cues for synapse specificity. Yet, we know little about how they guide the stereotyped organization of neural circuits. Advances in transcriptomics, genetic manipulations, neural tracing and imaging in intact nervous systems enable new avenues to identify mechanisms by which adhesion molecules regulate synapse specificity. Here we discuss the Cadherin superfamily, which forms one of the most functionally versatile families of cell adhesion molecules. Focusing on the classical cadherins and clustered protocadherins, we discuss recent findings that demonstrate roles in regulating synaptic partnerships and signaling properties, and optimizing neurite wiring. We highlight studies that demonstrate instructive roles through genetic manipulations with assays of synaptic connectivity. Understanding how neurons leverage a Cadherin code for specifying neural connectivity provides insights into the broader principles of circuit assembly and function.
{"title":"Cracking the cadherin codes that wire the nervous system","authors":"Madison T. Gray , Julie L. Lefebvre","doi":"10.1016/j.conb.2025.103086","DOIUrl":"10.1016/j.conb.2025.103086","url":null,"abstract":"<div><div>Synaptic partner recognition and precise connectivity are essential components of neural circuit formation and function. Cell adhesion molecules with selective binding properties provide instructive cues for synapse specificity. Yet, we know little about how they guide the stereotyped organization of neural circuits. Advances in transcriptomics, genetic manipulations, neural tracing and imaging in intact nervous systems enable new avenues to identify mechanisms by which adhesion molecules regulate synapse specificity. Here we discuss the Cadherin superfamily, which forms one of the most functionally versatile families of cell adhesion molecules. Focusing on the classical cadherins and clustered protocadherins, we discuss recent findings that demonstrate roles in regulating synaptic partnerships and signaling properties, and optimizing neurite wiring. We highlight studies that demonstrate instructive roles through genetic manipulations with assays of synaptic connectivity. Understanding how neurons leverage a Cadherin code for specifying neural connectivity provides insights into the broader principles of circuit assembly and function.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103086"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144570878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The reciprocal regulation of the neural ensemble and vascular network within the mammalian central nervous system (CNS) is crucial for its development and functionality. Neuron-derived pro-angiogenic factors, such as growth factors, morphogens, and guidance cues, play a key role in forming stereotypical vascular architectures in the cortex, spinal cord, and cerebellum during development. Notably, the CNS vasculature forms distinct 3D lattice structures composed of laminar vascular networks interconnected by penetrating vessels. This contrasts with the more random 3D arborizations found in tumors. While the morphogen gradients for vascular network growth have been well-studied, the mechanisms contributing to vascular patterning and lattice maintenance in 3D are not fully understood. The mammalian retina provides an ideal model for studying these mechanisms, given its laminar organization of neurons and plexus organization of vessels, allowing for the investigation of 2D growth to 3D lattice establishment in a stepwise manner. Notably, recent studies have highlighted the roles of neurons and glia in retinal vascular patterning in 2D, as well as the involvement of neurotransmitters in regulating vascular growth. Additionally, direct neuron-to-vessel interactions have been found to contribute to 3D retinal vascular lattice formation. As emerging technologies provide new insights into retinal vascular assembly in 3D, understanding the developmental regulation and the physiological and pathophysiological effects of 3D lattice disruption remains a fertile field of research.
{"title":"A neurobiology perspective on the assembly of retinal vasculature from 2D to 3D","authors":"Mahima Bose , Mengya Zhao , Kenichi Toma , Xin Ye , Xin Duan","doi":"10.1016/j.conb.2025.103085","DOIUrl":"10.1016/j.conb.2025.103085","url":null,"abstract":"<div><div>The reciprocal regulation of the neural ensemble and vascular network within the mammalian central nervous system (CNS) is crucial for its development and functionality. Neuron-derived pro-angiogenic factors, such as growth factors, morphogens, and guidance cues, play a key role in forming stereotypical vascular architectures in the cortex, spinal cord, and cerebellum during development. Notably, the CNS vasculature forms distinct 3D lattice structures composed of laminar vascular networks interconnected by penetrating vessels. This contrasts with the more random 3D arborizations found in tumors. While the morphogen gradients for vascular network growth have been well-studied, the mechanisms contributing to vascular patterning and lattice maintenance in 3D are not fully understood. The mammalian retina provides an ideal model for studying these mechanisms, given its laminar organization of neurons and plexus organization of vessels, allowing for the investigation of 2D growth to 3D lattice establishment in a stepwise manner. Notably, recent studies have highlighted the roles of neurons and glia in retinal vascular patterning in 2D, as well as the involvement of neurotransmitters in regulating vascular growth. Additionally, direct neuron-to-vessel interactions have been found to contribute to 3D retinal vascular lattice formation. As emerging technologies provide new insights into retinal vascular assembly in 3D, understanding the developmental regulation and the physiological and pathophysiological effects of 3D lattice disruption remains a fertile field of research.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103085"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144631574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-04-12DOI: 10.1016/j.conb.2025.103019
Jeffrey P. Gavornik , Mark F. Bear
Despite the explosion of high-tech methods to measure activity in the mouse visual cortex, the venerable visually evoked potential (VEP) continues to prove its worth as a sensitive measure of experience-dependent cortical plasticity. The VEP recorded in layer 4 is a good estimate of the strength of feedforward synaptic excitation, and changes in amplitude correspond closely to changes in the peak firing rate of principal cells. Chronic recording of VEPs in awake mice have enabled longitudinal study of modifications induced by selective visual experience or deprivation, and these have revealed several novel forms of plasticity. The VEP provides a good estimate of spatial acuity that compares well with values obtained by behavioral approaches. Furthermore, recordings of the local field potential through the same electrodes reveal changes in oscillatory activity that reflect differential recruitment of inhibitory networks. Thus, the VEP remains a powerful tool for the study of visual cortical plasticity.
{"title":"The visual evoked potential is a sensitive and powerful measure of experience-dependent visual cortical plasticity in mice","authors":"Jeffrey P. Gavornik , Mark F. Bear","doi":"10.1016/j.conb.2025.103019","DOIUrl":"10.1016/j.conb.2025.103019","url":null,"abstract":"<div><div>Despite the explosion of high-tech methods to measure activity in the mouse visual cortex, the venerable visually evoked potential (VEP) continues to prove its worth as a sensitive measure of experience-dependent cortical plasticity. The VEP recorded in layer 4 is a good estimate of the strength of feedforward synaptic excitation, and changes in amplitude correspond closely to changes in the peak firing rate of principal cells. Chronic recording of VEPs in awake mice have enabled longitudinal study of modifications induced by selective visual experience or deprivation, and these have revealed several novel forms of plasticity. The VEP provides a good estimate of spatial acuity that compares well with values obtained by behavioral approaches. Furthermore, recordings of the local field potential through the same electrodes reveal changes in oscillatory activity that reflect differential recruitment of inhibitory networks. Thus, the VEP remains a powerful tool for the study of visual cortical plasticity.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143820344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Interoception, or the perception and regulation of body signals by the central nervous system, is critical for maintaining homeostasis and coordination of behaviors. Deciphering the mechanisms of interoception requires identifying pathways and decoding of diverse signals across the brain-body axis. These studies are enabled by tools to modulate and record physiological processes in the brain and visceral organs. While numerous advanced neurotechnologies are well-established in the brain, these techniques often offer limited utility for other organs, such as the gastrointestinal tract, heart, liver, or bladder. In this review, we highlight recent advances in technologies for recording and modulation of visceral organ physiology in small animals in vivo, with a focus on implantable bioelectronic organ interfaces that can be deployed in behaving animals. We discuss how such interfaces are made possible through innovations in materials and electronics and outline unmet technological challenges in interoception research.
{"title":"Accessing the viscera: Technologies for interoception research","authors":"Karen K.L. Pang , Rajib Mondal , Atharva Sahasrabudhe , Polina Anikeeva","doi":"10.1016/j.conb.2025.103050","DOIUrl":"10.1016/j.conb.2025.103050","url":null,"abstract":"<div><div>Interoception, or the perception and regulation of body signals by the central nervous system, is critical for maintaining homeostasis and coordination of behaviors. Deciphering the mechanisms of interoception requires identifying pathways and decoding of diverse signals across the brain-body axis. These studies are enabled by tools to modulate and record physiological processes in the brain and visceral organs. While numerous advanced neurotechnologies are well-established in the brain, these techniques often offer limited utility for other organs, such as the gastrointestinal tract, heart, liver, or bladder. In this review, we highlight recent advances in technologies for recording and modulation of visceral organ physiology in small animals <em>in vivo,</em> with a focus on implantable bioelectronic organ interfaces that can be deployed in behaving animals. We discuss how such interfaces are made possible through innovations in materials and electronics and outline unmet technological challenges in interoception research.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103050"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144070737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}