Pub Date : 2025-03-24DOI: 10.1038/s41583-025-00914-5
Marzia Malcangio, George Sideris-Lampretsas
Neuropathic pain is a debilitating condition caused by damage to the nervous system that results in changes along the pain pathway that lead to persistence of the pain sensation. Unremitting pain conditions are associated with maladaptive plasticity, disruption of neuronal activity that favours excitation over inhibition, and engagement of immune cells. The substantial progress made over the last two decades in the neuroimmune interaction research area points to a mechanistic role of spinal cord microglia, which are resident immune cells of the CNS. Microglia respond to and modulate neuronal activity during establishment and persistence of neuropathic pain states, and microglia–neuron pathways provide targets that can be exploited to attenuate abnormal neuronal activity and provide pain relief. Neuropathic pain caused by nerve damage results in neuronal pathway changes and immune cell engagement. In this Review, Malcangio and Sideris-Lampretsas discuss how microglia respond to and modulate neuronal activity and suggest that microglia–neuron pathways offer novel approaches for the attenuation of neuropathic pain.
{"title":"How microglia contribute to the induction and maintenance of neuropathic pain","authors":"Marzia Malcangio, George Sideris-Lampretsas","doi":"10.1038/s41583-025-00914-5","DOIUrl":"10.1038/s41583-025-00914-5","url":null,"abstract":"Neuropathic pain is a debilitating condition caused by damage to the nervous system that results in changes along the pain pathway that lead to persistence of the pain sensation. Unremitting pain conditions are associated with maladaptive plasticity, disruption of neuronal activity that favours excitation over inhibition, and engagement of immune cells. The substantial progress made over the last two decades in the neuroimmune interaction research area points to a mechanistic role of spinal cord microglia, which are resident immune cells of the CNS. Microglia respond to and modulate neuronal activity during establishment and persistence of neuropathic pain states, and microglia–neuron pathways provide targets that can be exploited to attenuate abnormal neuronal activity and provide pain relief. Neuropathic pain caused by nerve damage results in neuronal pathway changes and immune cell engagement. In this Review, Malcangio and Sideris-Lampretsas discuss how microglia respond to and modulate neuronal activity and suggest that microglia–neuron pathways offer novel approaches for the attenuation of neuropathic pain.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 5","pages":"263-275"},"PeriodicalIF":26.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143677653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-20DOI: 10.1038/s41583-025-00916-3
Jade S. Duffy, Mark A. Bellgrove, Peter R. Murphy, Redmond G. O’Connell
Even the most highly-trained observers presented with identical choice-relevant stimuli will reliably exhibit substantial trial-to-trial variability in the timing and accuracy of their choices. Despite being a pervasive feature of choice behaviour and a prominent phenotype for numerous clinical disorders, the capability to disentangle the sources of such intra-individual variability (IIV) remains limited. In principle, computational models of decision-making offer a means of parsing and estimating these sources, but methodological limitations have prevented this potential from being fully realized in practice. In this Review, we first discuss current limitations of algorithmic models for understanding variability in decision-making behaviour. We then highlight recent advances in behavioural paradigm design, novel analyses of cross-trial behavioural and neural dynamics, and the development of neurally grounded computational models that are now making it possible to link distinct components of IIV to well-defined neural processes. Taken together, we demonstrate how these methods are opening up new avenues for systematically analysing the neural origins of IIV, paving the way for a more refined, holistic understanding of decision-making in health and disease. Identifying the psychological and neurobiological processes underpinning intra-individual variations in choice behaviour presents a formidable challenge. In this Review, Duffy et al. discuss how algorithmic models for teasing apart such sources of variability and advances in behavioural paradigm design and neurally grounded computational modelling are providing new avenues for systematic progress.
{"title":"Disentangling sources of variability in decision-making","authors":"Jade S. Duffy, Mark A. Bellgrove, Peter R. Murphy, Redmond G. O’Connell","doi":"10.1038/s41583-025-00916-3","DOIUrl":"10.1038/s41583-025-00916-3","url":null,"abstract":"Even the most highly-trained observers presented with identical choice-relevant stimuli will reliably exhibit substantial trial-to-trial variability in the timing and accuracy of their choices. Despite being a pervasive feature of choice behaviour and a prominent phenotype for numerous clinical disorders, the capability to disentangle the sources of such intra-individual variability (IIV) remains limited. In principle, computational models of decision-making offer a means of parsing and estimating these sources, but methodological limitations have prevented this potential from being fully realized in practice. In this Review, we first discuss current limitations of algorithmic models for understanding variability in decision-making behaviour. We then highlight recent advances in behavioural paradigm design, novel analyses of cross-trial behavioural and neural dynamics, and the development of neurally grounded computational models that are now making it possible to link distinct components of IIV to well-defined neural processes. Taken together, we demonstrate how these methods are opening up new avenues for systematically analysing the neural origins of IIV, paving the way for a more refined, holistic understanding of decision-making in health and disease. Identifying the psychological and neurobiological processes underpinning intra-individual variations in choice behaviour presents a formidable challenge. In this Review, Duffy et al. discuss how algorithmic models for teasing apart such sources of variability and advances in behavioural paradigm design and neurally grounded computational modelling are providing new avenues for systematic progress.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 5","pages":"247-262"},"PeriodicalIF":26.7,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143660546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-18DOI: 10.1038/s41583-025-00915-4
Eleanor E. Harding, Ji Chul Kim, Alexander P. Demos, Iran R. Roman, Parker Tichko, Caroline Palmer, Edward W. Large
A great deal of research in the neuroscience of music suggests that neural oscillations synchronize with musical stimuli. Although neural synchronization is a well-studied mechanism underpinning expectation, it has even more far-reaching implications for music. In this Perspective, we survey the literature on the neuroscience of music, including pitch, harmony, melody, tonality, rhythm, metre, groove and affect. We describe how fundamental dynamical principles based on known neural mechanisms can explain basic aspects of music perception and performance, as summarized in neural resonance theory. Building on principles such as resonance, stability, attunement and strong anticipation, we propose that people anticipate musical events not through predictive neural models, but because brain–body dynamics physically embody musical structure. The interaction of certain kinds of sounds with ongoing pattern-forming dynamics results in patterns of perception, action and coordination that we collectively experience as music. Statistically universal structures may have arisen in music because they correspond to stable states of complex, pattern-forming dynamical systems. This analysis of empirical findings from the perspective of neurodynamic principles sheds new light on the neuroscience of music and what makes music powerful. In this Perspective article, Edward Large and colleagues examine the neuroscience of music, placing their focus on neural resonance theory, which summarizes how the dynamics of fundamental neural mechanisms can explain various aspects of music perception and performance.
{"title":"Musical neurodynamics","authors":"Eleanor E. Harding, Ji Chul Kim, Alexander P. Demos, Iran R. Roman, Parker Tichko, Caroline Palmer, Edward W. Large","doi":"10.1038/s41583-025-00915-4","DOIUrl":"10.1038/s41583-025-00915-4","url":null,"abstract":"A great deal of research in the neuroscience of music suggests that neural oscillations synchronize with musical stimuli. Although neural synchronization is a well-studied mechanism underpinning expectation, it has even more far-reaching implications for music. In this Perspective, we survey the literature on the neuroscience of music, including pitch, harmony, melody, tonality, rhythm, metre, groove and affect. We describe how fundamental dynamical principles based on known neural mechanisms can explain basic aspects of music perception and performance, as summarized in neural resonance theory. Building on principles such as resonance, stability, attunement and strong anticipation, we propose that people anticipate musical events not through predictive neural models, but because brain–body dynamics physically embody musical structure. The interaction of certain kinds of sounds with ongoing pattern-forming dynamics results in patterns of perception, action and coordination that we collectively experience as music. Statistically universal structures may have arisen in music because they correspond to stable states of complex, pattern-forming dynamical systems. This analysis of empirical findings from the perspective of neurodynamic principles sheds new light on the neuroscience of music and what makes music powerful. In this Perspective article, Edward Large and colleagues examine the neuroscience of music, placing their focus on neural resonance theory, which summarizes how the dynamics of fundamental neural mechanisms can explain various aspects of music perception and performance.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 5","pages":"293-307"},"PeriodicalIF":26.7,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143653339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-28DOI: 10.1038/s41583-025-00912-7
Sian Lewis
A possible mechanism underlying the worsening of asthma symptoms after eating is found in mice, where type 2 immunity in the lung (which is a primary driver of asthma) is found to be potentiated by food intake.
{"title":"How eating makes asthma worse","authors":"Sian Lewis","doi":"10.1038/s41583-025-00912-7","DOIUrl":"10.1038/s41583-025-00912-7","url":null,"abstract":"A possible mechanism underlying the worsening of asthma symptoms after eating is found in mice, where type 2 immunity in the lung (which is a primary driver of asthma) is found to be potentiated by food intake.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 4","pages":"193-193"},"PeriodicalIF":28.7,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143517815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-26DOI: 10.1038/s41583-025-00913-6
Jake Rogers
A modified looming paradigm teases apart how top-down cortical inputs from visual areas can override instinctive fear responses in mice via an endocannabinoid-mediated inhibitory plasticity mechanism in subcortical circuits.
{"title":"Sensory cortex quashes subcortical escape instinct","authors":"Jake Rogers","doi":"10.1038/s41583-025-00913-6","DOIUrl":"10.1038/s41583-025-00913-6","url":null,"abstract":"A modified looming paradigm teases apart how top-down cortical inputs from visual areas can override instinctive fear responses in mice via an endocannabinoid-mediated inhibitory plasticity mechanism in subcortical circuits.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 4","pages":"194-194"},"PeriodicalIF":28.7,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143495323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-24DOI: 10.1038/s41583-025-00910-9
Dániel L. Barabási, André Ferreira Castro, Florian Engert
Understanding the relationship between genotype and neuronal circuit phenotype necessitates an integrated view of genetics, development, plasticity and learning. Challenging the prevailing notion that emphasizes learning and plasticity as primary drivers of circuit assembly, in this Perspective, we delineate a tripartite framework to clarify the respective roles that learning and plasticity might have in this process. In the first part of the framework, which we term System One, neural circuits are established purely through genetically driven algorithms, in which spike timing-dependent plasticity serves no instructive role. We propose that these circuits equip the animal with sufficient skill and knowledge to successfully engage the world. Next, System Two is governed by rare but critical ‘single-shot learning’ events, which occur in response to survival situations and prompt rapid synaptic reconfiguration. Such events serve as crucial updates to the existing hardwired knowledge base of an organism. Finally, System Three is characterized by a perpetual state of synaptic recalibration, involving continual plasticity for circuit stabilization and fine-tuning. By outlining the definitions and roles of these three core systems, our framework aims to resolve existing ambiguities related to and enrich our understanding of neural circuit formation. In this Perspective, Barabási, Ferreira Castro and Engert challenge the notion that learning and plasticity primarily drive the assembly of neural circuits. They present a tripartite framework for how neural circuits form, outlining the relative contributions of developmental, associative learning and tuning-based factors to this process and knowledge acquisition.
{"title":"Three systems of circuit formation: assembly, updating and tuning","authors":"Dániel L. Barabási, André Ferreira Castro, Florian Engert","doi":"10.1038/s41583-025-00910-9","DOIUrl":"10.1038/s41583-025-00910-9","url":null,"abstract":"Understanding the relationship between genotype and neuronal circuit phenotype necessitates an integrated view of genetics, development, plasticity and learning. Challenging the prevailing notion that emphasizes learning and plasticity as primary drivers of circuit assembly, in this Perspective, we delineate a tripartite framework to clarify the respective roles that learning and plasticity might have in this process. In the first part of the framework, which we term System One, neural circuits are established purely through genetically driven algorithms, in which spike timing-dependent plasticity serves no instructive role. We propose that these circuits equip the animal with sufficient skill and knowledge to successfully engage the world. Next, System Two is governed by rare but critical ‘single-shot learning’ events, which occur in response to survival situations and prompt rapid synaptic reconfiguration. Such events serve as crucial updates to the existing hardwired knowledge base of an organism. Finally, System Three is characterized by a perpetual state of synaptic recalibration, involving continual plasticity for circuit stabilization and fine-tuning. By outlining the definitions and roles of these three core systems, our framework aims to resolve existing ambiguities related to and enrich our understanding of neural circuit formation. In this Perspective, Barabási, Ferreira Castro and Engert challenge the notion that learning and plasticity primarily drive the assembly of neural circuits. They present a tripartite framework for how neural circuits form, outlining the relative contributions of developmental, associative learning and tuning-based factors to this process and knowledge acquisition.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 4","pages":"232-243"},"PeriodicalIF":28.7,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143485670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-19DOI: 10.1038/s41583-025-00908-3
Sam Vanherle, Melanie Loix, Veronique E. Miron, Jerome J. A. Hendriks, Jeroen F. J. Bogie
Lipid metabolism encompasses the catabolism and anabolism of lipids, and is fundamental for the maintenance of cellular homeostasis, particularly within the lipid-rich CNS. Increasing evidence further underscores the importance of lipid remodelling and transfer within and between glial cells and neurons as key orchestrators of CNS lipid homeostasis. In this Review, we summarize and discuss the complex landscape of processes involved in lipid metabolism, remodelling and intercellular transfer in the CNS. Highlighted are key pathways, including those mediating lipid (and lipid droplet) biogenesis and breakdown, lipid oxidation and phospholipid metabolism, as well as cell–cell lipid transfer mediated via lipoproteins, extracellular vesicles and tunnelling nanotubes. We further explore how the dysregulation of these pathways contributes to the onset and progression of neurodegenerative diseases, and examine the homeostatic and pathogenic impacts of environment, diet and lifestyle on CNS lipid metabolism. Within the CNS, lipids have vital roles in numerous cellular functions and the maintenance of lipid homeostasis is essential for brain health. Bogie and colleagues explore the mechanisms that regulate lipid biogenesis, metabolism and remodelling in the CNS, the transfer of lipids between different CNS cell types and the impact of loss of lipid homeostasis in neurodegenerative diseases.
{"title":"Lipid metabolism, remodelling and intercellular transfer in the CNS","authors":"Sam Vanherle, Melanie Loix, Veronique E. Miron, Jerome J. A. Hendriks, Jeroen F. J. Bogie","doi":"10.1038/s41583-025-00908-3","DOIUrl":"10.1038/s41583-025-00908-3","url":null,"abstract":"Lipid metabolism encompasses the catabolism and anabolism of lipids, and is fundamental for the maintenance of cellular homeostasis, particularly within the lipid-rich CNS. Increasing evidence further underscores the importance of lipid remodelling and transfer within and between glial cells and neurons as key orchestrators of CNS lipid homeostasis. In this Review, we summarize and discuss the complex landscape of processes involved in lipid metabolism, remodelling and intercellular transfer in the CNS. Highlighted are key pathways, including those mediating lipid (and lipid droplet) biogenesis and breakdown, lipid oxidation and phospholipid metabolism, as well as cell–cell lipid transfer mediated via lipoproteins, extracellular vesicles and tunnelling nanotubes. We further explore how the dysregulation of these pathways contributes to the onset and progression of neurodegenerative diseases, and examine the homeostatic and pathogenic impacts of environment, diet and lifestyle on CNS lipid metabolism. Within the CNS, lipids have vital roles in numerous cellular functions and the maintenance of lipid homeostasis is essential for brain health. Bogie and colleagues explore the mechanisms that regulate lipid biogenesis, metabolism and remodelling in the CNS, the transfer of lipids between different CNS cell types and the impact of loss of lipid homeostasis in neurodegenerative diseases.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 4","pages":"214-231"},"PeriodicalIF":28.7,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143443321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-06DOI: 10.1038/s41583-025-00906-5
Murielle Saade, Elisa Martí
As one of the simplest and most evolutionarily conserved parts of the vertebrate nervous system, the spinal cord serves as a key model for understanding the principles of nervous system construction. During embryonic development, the spinal cord originates from a population of bipotent stem cells termed neuromesodermal progenitors, which are organized within a transient embryonic structure known as the neural tube. Neural tube morphogenesis differs along its anterior-to-posterior axis: most of the neural tube (including the regions that will develop into the brain and the anterior spinal cord) forms via the bending and dorsal fusion of the neural groove, but the establishment of the posterior region of the neural tube involves de novo formation of a lumen within a solid medullary cord. The early spinal cord primordium consists of highly polarized neural progenitor cells organized into a pseudostratified epithelium. Tight regulation of the cell division modes of these progenitors drives the embryonic growth of the neural tube and initiates primary neurogenesis. A rich history of observational and functional studies across various vertebrate models has advanced our understanding of the cellular events underlying spinal cord development, and these foundational studies are beginning to inform our knowledge of human spinal cord development. During vertebrate embryonic development, the spinal cord emerges from the posterior portion of the neural tube. Saade and Martí describe the complex series of morphogenetic events that shape the neural tube and the cellular and molecular mechanisms that regulate the formation of the embryonic spinal cord.
{"title":"Early spinal cord development: from neural tube formation to neurogenesis","authors":"Murielle Saade, Elisa Martí","doi":"10.1038/s41583-025-00906-5","DOIUrl":"10.1038/s41583-025-00906-5","url":null,"abstract":"As one of the simplest and most evolutionarily conserved parts of the vertebrate nervous system, the spinal cord serves as a key model for understanding the principles of nervous system construction. During embryonic development, the spinal cord originates from a population of bipotent stem cells termed neuromesodermal progenitors, which are organized within a transient embryonic structure known as the neural tube. Neural tube morphogenesis differs along its anterior-to-posterior axis: most of the neural tube (including the regions that will develop into the brain and the anterior spinal cord) forms via the bending and dorsal fusion of the neural groove, but the establishment of the posterior region of the neural tube involves de novo formation of a lumen within a solid medullary cord. The early spinal cord primordium consists of highly polarized neural progenitor cells organized into a pseudostratified epithelium. Tight regulation of the cell division modes of these progenitors drives the embryonic growth of the neural tube and initiates primary neurogenesis. A rich history of observational and functional studies across various vertebrate models has advanced our understanding of the cellular events underlying spinal cord development, and these foundational studies are beginning to inform our knowledge of human spinal cord development. During vertebrate embryonic development, the spinal cord emerges from the posterior portion of the neural tube. Saade and Martí describe the complex series of morphogenetic events that shape the neural tube and the cellular and molecular mechanisms that regulate the formation of the embryonic spinal cord.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 4","pages":"195-213"},"PeriodicalIF":28.7,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143258098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-02-05DOI: 10.1038/s41583-025-00909-2
Katherine Whalley
A study explores the sexually dimorphic circuits that regulate sociosexual preferences in mice.
一项研究探索了调节小鼠社会性偏好的两性二态电路。
{"title":"Pathways to sex preferences","authors":"Katherine Whalley","doi":"10.1038/s41583-025-00909-2","DOIUrl":"10.1038/s41583-025-00909-2","url":null,"abstract":"A study explores the sexually dimorphic circuits that regulate sociosexual preferences in mice.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 4","pages":"193-193"},"PeriodicalIF":28.7,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143124760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-29DOI: 10.1038/s41583-025-00907-4
Darran Yates
A new study reveals distinct circuit features of the human hippocampal CA3 region.
一项新的研究揭示了人类海马CA3区域的独特电路特征。
{"title":"Human hippocampal circuit characterization","authors":"Darran Yates","doi":"10.1038/s41583-025-00907-4","DOIUrl":"10.1038/s41583-025-00907-4","url":null,"abstract":"A new study reveals distinct circuit features of the human hippocampal CA3 region.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 3","pages":"138-138"},"PeriodicalIF":28.7,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143057107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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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