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":"2025-10-01","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 : 2025-10-01Epub Date: 2025-08-16DOI: 10.1016/j.conb.2025.103096
Nilay Yapici
Over the past decades, significant advancements have transformed our understanding of the gut-brain circuits in Drosophila melanogaster. In this review, we explore how mapping these circuits and signaling pathways has deepened our knowledge of the neural and hormonal pathways that regulate nutrient preference, feeding behavior, metabolism, and other homeostatic behaviors in flies. We summarize the recent breakthroughs in gut-brain communication and highlight how these advancements have provided valuable insights into the complex relationship between the gut and the brain. Finally, we emphasize the importance of Drosophila as a model system for investigating gut-brain communication. Insights from fly research not only enhance our understanding of fundamental gut-brain biology but also provide promising avenues for identifying molecular targets for therapeutic strategies in humans for gastrointestinal and metabolic disorders.
{"title":"Gut-brain communication in Drosophila melanogaster","authors":"Nilay Yapici","doi":"10.1016/j.conb.2025.103096","DOIUrl":"10.1016/j.conb.2025.103096","url":null,"abstract":"<div><div>Over the past decades, significant advancements have transformed our understanding of the gut-brain circuits in <em>Drosophila melanogaster</em>. In this review, we explore how mapping these circuits and signaling pathways has deepened our knowledge of the neural and hormonal pathways that regulate nutrient preference, feeding behavior, metabolism, and other homeostatic behaviors in flies. We summarize the recent breakthroughs in gut-brain communication and highlight how these advancements have provided valuable insights into the complex relationship between the gut and the brain. Finally, we emphasize the importance of <em>Drosophila</em> as a model system for investigating gut-brain communication. Insights from fly research not only enhance our understanding of fundamental gut-brain biology but also provide promising avenues for identifying molecular targets for therapeutic strategies in humans for gastrointestinal and metabolic disorders.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"94 ","pages":"Article 103096"},"PeriodicalIF":5.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144852823","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 : 2025-10-01Epub Date: 2025-08-16DOI: 10.1016/j.conb.2025.103093
Kathryn L. Todd , Kaitlyn M.L. Cramb , Katherine R. Brimblecombe , Stephanie J. Cragg
Dopamine release in the striatum is credited with being critical to the selection and learning of motivated actions and outcomes. Dysregulation of striatal dopamine release underlies multiple disorders of action selection and reward-processing, such as Parkinson’s disease, schizophrenia and addiction disorders, and is a major target for therapeutic interventions. The axonal molecular and circuit mechanisms governing dopamine exocytosis are incompletely resolved, but accumulating evidence suggests some key points of divergence from canonical neurotransmitter synapses. In this review, we bring together recent insights into mechanisms shaping dopamine transmission in the striatum, spanning the molecular machinery regulating exocytosis, striatal modulators locally governing release probability, and the mechanisms regulating dopamine vesicle endocytosis. Together, these findings continue to support points of divergence from canonical presynaptic mechanisms, they inform principles of axonal neuromodulation, and point to potential contributions to the susceptibility to neurodegeneration in Parkinson’s disease.
{"title":"New insights into axonal regulators of dopamine transmission in health and disease","authors":"Kathryn L. Todd , Kaitlyn M.L. Cramb , Katherine R. Brimblecombe , Stephanie J. Cragg","doi":"10.1016/j.conb.2025.103093","DOIUrl":"10.1016/j.conb.2025.103093","url":null,"abstract":"<div><div>Dopamine release in the striatum is credited with being critical to the selection and learning of motivated actions and outcomes. Dysregulation of striatal dopamine release underlies multiple disorders of action selection and reward-processing, such as Parkinson’s disease, schizophrenia and addiction disorders, and is a major target for therapeutic interventions. The axonal molecular and circuit mechanisms governing dopamine exocytosis are incompletely resolved, but accumulating evidence suggests some key points of divergence from canonical neurotransmitter synapses. In this review, we bring together recent insights into mechanisms shaping dopamine transmission in the striatum, spanning the molecular machinery regulating exocytosis, striatal modulators locally governing release probability, and the mechanisms regulating dopamine vesicle endocytosis. Together, these findings continue to support points of divergence from canonical presynaptic mechanisms, they inform principles of axonal neuromodulation, and point to potential contributions to the susceptibility to neurodegeneration in Parkinson’s disease.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"94 ","pages":"Article 103093"},"PeriodicalIF":5.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144858177","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 : 2025-10-01Epub Date: 2025-08-28DOI: 10.1016/j.conb.2025.103105
Silvia Rodriguez-Rozada , Philip Tovote
Dynamic cardiovascular control supports adaptive behavior under external and internal influences. Higher-order brain regions regulate stress-related cardiovascular changes via their influence on medullary nuclei, which control autonomic reflexes. Despite extensive research, the precise neural circuits linking cardiac function and behavior under emotional stress remain unclear. This review highlights recent studies identifying specific cell types and pathways involved in cardiovascular regulation, emphasizing their dynamical role under baseline and threat conditions. Cardiovascular responses are closely tied to behavior through descending brain-to-heart command pathways and ascending interoceptive feedback. Our framework for characterizing cardio-behavioral states under threat identifies rapid-acting “microstates” and slow-changing “macrostates” reflecting context- and time-dependent threat levels. Multidimensional measurements and integrated analytical approaches are required to study neural circuits controlling cardio-behavioral states. Understanding the homeodynamic regulation of cardiac function and its behavioral links is essential for unraveling brain-heart interactions.
{"title":"Central regulation of cardio-behavioral responses: Circuit engagement during aversive emotional states","authors":"Silvia Rodriguez-Rozada , Philip Tovote","doi":"10.1016/j.conb.2025.103105","DOIUrl":"10.1016/j.conb.2025.103105","url":null,"abstract":"<div><div>Dynamic cardiovascular control supports adaptive behavior under external and internal influences. Higher-order brain regions regulate stress-related cardiovascular changes via their influence on medullary nuclei, which control autonomic reflexes. Despite extensive research, the precise neural circuits linking cardiac function and behavior under emotional stress remain unclear. This review highlights recent studies identifying specific cell types and pathways involved in cardiovascular regulation, emphasizing their dynamical role under baseline and threat conditions. Cardiovascular responses are closely tied to behavior through descending brain-to-heart command pathways and ascending interoceptive feedback. Our framework for characterizing cardio-behavioral states under threat identifies rapid-acting “microstates” and slow-changing “macrostates” reflecting context- and time-dependent threat levels. Multidimensional measurements and integrated analytical approaches are required to study neural circuits controlling cardio-behavioral states. Understanding the homeodynamic regulation of cardiac function and its behavioral links is essential for unraveling brain-heart interactions.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"94 ","pages":"Article 103105"},"PeriodicalIF":5.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144908293","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: 2025-06-25DOI: 10.1016/j.conb.2025.103067
Rose Z. Hill
The kidneys filter the blood and balance fluid and electrolytes to keep the composition of the internal environment within the narrow parameters essential for life. A perturbation to the internal state, such as a sudden loss of blood or dehydration, engages autonomic efferent and neuroendocrine pathways to adjust kidney function rapidly and robustly. The mechanisms of these multiorgan pathways are extensively studied. By contrast, the roles of sensory afferent nerves in regulating renal function are just beginning to be understood. In this review, we examine recent advances in understanding the morphology, identity, and functions of the renal sensory nerves that form the first node in the interoceptive pathways that update the kidney on its own internal state. We end by highlighting open questions in the field, influenced by recent work in other areas of interoception neuroscience, and the outstanding gaps in our knowledge of kidney biology.
{"title":"Renal interoception: form, function, and open questions","authors":"Rose Z. Hill","doi":"10.1016/j.conb.2025.103067","DOIUrl":"10.1016/j.conb.2025.103067","url":null,"abstract":"<div><div>The kidneys filter the blood and balance fluid and electrolytes to keep the composition of the internal environment within the narrow parameters essential for life. A perturbation to the internal state, such as a sudden loss of blood or dehydration, engages autonomic efferent and neuroendocrine pathways to adjust kidney function rapidly and robustly. The mechanisms of these multiorgan pathways are extensively studied. By contrast, the roles of sensory afferent nerves in regulating renal function are just beginning to be understood. In this review, we examine recent advances in understanding the morphology, identity, and functions of the renal sensory nerves that form the first node in the interoceptive pathways that update the kidney on its own internal state. We end by highlighting open questions in the field, influenced by recent work in other areas of interoception neuroscience, and the outstanding gaps in our knowledge of kidney biology.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103067"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144470338","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: 2025-06-09DOI: 10.1016/j.conb.2025.103063
Clare E. Hancock , Binod Aryal , Tianji Ma , Guangyan Wu , Qili Liu
Feeding behaviors are driven not just by caloric needs but also by nutrient-specific appetites, which guide animals to seek out foods that correct specific nutritional deficiencies and fulfill diverse nutrient requirements. Despite the longstanding behavioral manifestations of nutrient-specific appetites for various nutrients, progress in understanding the underlying mechanisms has been slow. In this review, we summarize the challenges and recent advances in the study of nutrient-specific appetites for macronutrients and micronutrients, focusing on sodium- and protein-specific hunger. We examine central mechanisms that integrate peripheral, interceptive, and internal state signals to drive nutrient-specific preference and ingestion. We also explore conserved features and interactions across different nutrient-specific appetites, and discuss their implications for future research.
{"title":"Targeted cravings: Unraveling the drivers of nutrient-specific appetite","authors":"Clare E. Hancock , Binod Aryal , Tianji Ma , Guangyan Wu , Qili Liu","doi":"10.1016/j.conb.2025.103063","DOIUrl":"10.1016/j.conb.2025.103063","url":null,"abstract":"<div><div>Feeding behaviors are driven not just by caloric needs but also by nutrient-specific appetites, which guide animals to seek out foods that correct specific nutritional deficiencies and fulfill diverse nutrient requirements. Despite the longstanding behavioral manifestations of nutrient-specific appetites for various nutrients, progress in understanding the underlying mechanisms has been slow. In this review, we summarize the challenges and recent advances in the study of nutrient-specific appetites for macronutrients and micronutrients, focusing on sodium- and protein-specific hunger. We examine central mechanisms that integrate peripheral, interceptive, and internal state signals to drive nutrient-specific preference and ingestion. We also explore conserved features and interactions across different nutrient-specific appetites, and discuss their implications for future research.</div></div>","PeriodicalId":10999,"journal":{"name":"Current Opinion in Neurobiology","volume":"93 ","pages":"Article 103063"},"PeriodicalIF":4.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144241831","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}
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