Pub Date : 2024-07-24DOI: 10.1038/s41583-024-00848-4
Katherine Whalley
Cerebellar Purkinje neurons modulate thirst in mice
小脑浦肯野神经元调节小鼠的渴感
{"title":"Thirsty work for the cerebellum","authors":"Katherine Whalley","doi":"10.1038/s41583-024-00848-4","DOIUrl":"10.1038/s41583-024-00848-4","url":null,"abstract":"Cerebellar Purkinje neurons modulate thirst in mice","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 9","pages":"593-593"},"PeriodicalIF":28.7,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141754749","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 : 2024-07-19DOI: 10.1038/s41583-024-00837-7
Patrick F. Sullivan, Shuyang Yao, Jens Hjerling-Leffler
Determining the causes of schizophrenia has been a notoriously intractable problem, resistant to a multitude of investigative approaches over centuries. In recent decades, genomic studies have delivered hundreds of robust findings that implicate nearly 300 common genetic variants (via genome-wide association studies) and more than 20 rare variants (via whole-exome sequencing and copy number variant studies) as risk factors for schizophrenia. In parallel, functional genomic and neurobiological studies have provided exceptionally detailed information about the cellular composition of the brain and its interconnections in neurotypical individuals and, increasingly, in those with schizophrenia. Taken together, these results suggest unexpected complexity in the mechanisms that drive schizophrenia, pointing to the involvement of ensembles of genes (polygenicity) rather than single-gene causation. In this Review, we describe what we now know about the genetics of schizophrenia and consider the neurobiological implications of this information. In recent years, genomic studies have identified numerous genetic variants as risk factors for schizophrenia. Sullivan et al. describe our current understanding of the complex genetic architecture of schizophrenia and consider how the genomic findings can be interrogated to boost our understanding of the neurobiology of the disorder.
{"title":"Schizophrenia genomics: genetic complexity and functional insights","authors":"Patrick F. Sullivan, Shuyang Yao, Jens Hjerling-Leffler","doi":"10.1038/s41583-024-00837-7","DOIUrl":"10.1038/s41583-024-00837-7","url":null,"abstract":"Determining the causes of schizophrenia has been a notoriously intractable problem, resistant to a multitude of investigative approaches over centuries. In recent decades, genomic studies have delivered hundreds of robust findings that implicate nearly 300 common genetic variants (via genome-wide association studies) and more than 20 rare variants (via whole-exome sequencing and copy number variant studies) as risk factors for schizophrenia. In parallel, functional genomic and neurobiological studies have provided exceptionally detailed information about the cellular composition of the brain and its interconnections in neurotypical individuals and, increasingly, in those with schizophrenia. Taken together, these results suggest unexpected complexity in the mechanisms that drive schizophrenia, pointing to the involvement of ensembles of genes (polygenicity) rather than single-gene causation. In this Review, we describe what we now know about the genetics of schizophrenia and consider the neurobiological implications of this information. In recent years, genomic studies have identified numerous genetic variants as risk factors for schizophrenia. Sullivan et al. describe our current understanding of the complex genetic architecture of schizophrenia and consider how the genomic findings can be interrogated to boost our understanding of the neurobiology of the disorder.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 9","pages":"611-624"},"PeriodicalIF":28.7,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141727583","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 : 2024-07-16DOI: 10.1038/s41583-024-00847-5
Xiao-Jing Wang
{"title":"Publisher Correction: Macroscopic gradients of synaptic excitation and inhibition in the neocortex","authors":"Xiao-Jing Wang","doi":"10.1038/s41583-024-00847-5","DOIUrl":"10.1038/s41583-024-00847-5","url":null,"abstract":"","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 9","pages":"643-643"},"PeriodicalIF":28.7,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41583-024-00847-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141627204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-08DOI: 10.1038/s41583-024-00844-8
Darran Yates
Acid-sensing ion channel 3 in nociceptors exacerbates inflammation in psoriasis by inducing the release of calcitonin gene-related peptide from these neurons.
痛觉感受器中的酸感应离子通道 3 通过诱导这些神经元释放降钙素基因相关肽而加剧牛皮癣的炎症。
{"title":"Neurogenic exacerbation of psoriasis","authors":"Darran Yates","doi":"10.1038/s41583-024-00844-8","DOIUrl":"10.1038/s41583-024-00844-8","url":null,"abstract":"Acid-sensing ion channel 3 in nociceptors exacerbates inflammation in psoriasis by inducing the release of calcitonin gene-related peptide from these neurons.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 8","pages":"516-516"},"PeriodicalIF":28.7,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141556738","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 : 2024-07-02DOI: 10.1038/s41583-024-00842-w
Jake Rogers
A new modelling method developed in male Drosophila melanogaster maps how populations of neurons transform visual stimuli into courtship behaviours without recording neural activity.
{"title":"Predicting natural behaviour by perturbation","authors":"Jake Rogers","doi":"10.1038/s41583-024-00842-w","DOIUrl":"10.1038/s41583-024-00842-w","url":null,"abstract":"A new modelling method developed in male Drosophila melanogaster maps how populations of neurons transform visual stimuli into courtship behaviours without recording neural activity.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 8","pages":"516-516"},"PeriodicalIF":28.7,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141492784","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 : 2024-07-01DOI: 10.1038/s41583-024-00833-x
Stefan Thor
During central nervous system (CNS) development, neural progenitor cells (NPCs) generate neurons and glia in two different ways. In direct neurogenesis, daughter cells differentiate directly into neurons or glia, whereas in indirect neurogenesis, neurons or glia are generated after one or more daughter cell divisions. Intriguingly, indirect neurogenesis is not stochastically deployed and plays instructive roles during CNS development: increased generation of cells from specific lineages; increased generation of early or late-born cell types within a lineage; and increased cell diversification. Increased indirect neurogenesis might contribute to the anterior CNS expansion evident throughout the Bilateria and help to modify brain-region size without requiring increased NPC numbers or extended neurogenesis. Increased indirect neurogenesis could be an evolutionary driver of the gyrencephalic (that is, folded) cortex that emerged during mammalian evolution and might even have increased during hominid evolution. Thus, selection of indirect versus direct neurogenesis provides a powerful developmental and evolutionary instrument that drives not only the evolution of CNS complexity but also brain expansion and modulation of brain-region size, and thereby the evolution of increasingly advanced cognitive abilities. This Review describes indirect neurogenesis in several model species and humans, and highlights some of the molecular genetic mechanisms that control this important process. Central nervous system (CNS) neurons and glial cells are generated by both direct and indirect neurogenesis. In this Review, Thor outlines the landscape of indirect neurogenesis during CNS development in key species, including humans, and describes the main genetic mechanisms that contribute to its region-specific, neural progenitor cell-specific and temporal control.
{"title":"Indirect neurogenesis in space and time","authors":"Stefan Thor","doi":"10.1038/s41583-024-00833-x","DOIUrl":"10.1038/s41583-024-00833-x","url":null,"abstract":"During central nervous system (CNS) development, neural progenitor cells (NPCs) generate neurons and glia in two different ways. In direct neurogenesis, daughter cells differentiate directly into neurons or glia, whereas in indirect neurogenesis, neurons or glia are generated after one or more daughter cell divisions. Intriguingly, indirect neurogenesis is not stochastically deployed and plays instructive roles during CNS development: increased generation of cells from specific lineages; increased generation of early or late-born cell types within a lineage; and increased cell diversification. Increased indirect neurogenesis might contribute to the anterior CNS expansion evident throughout the Bilateria and help to modify brain-region size without requiring increased NPC numbers or extended neurogenesis. Increased indirect neurogenesis could be an evolutionary driver of the gyrencephalic (that is, folded) cortex that emerged during mammalian evolution and might even have increased during hominid evolution. Thus, selection of indirect versus direct neurogenesis provides a powerful developmental and evolutionary instrument that drives not only the evolution of CNS complexity but also brain expansion and modulation of brain-region size, and thereby the evolution of increasingly advanced cognitive abilities. This Review describes indirect neurogenesis in several model species and humans, and highlights some of the molecular genetic mechanisms that control this important process. Central nervous system (CNS) neurons and glial cells are generated by both direct and indirect neurogenesis. In this Review, Thor outlines the landscape of indirect neurogenesis during CNS development in key species, including humans, and describes the main genetic mechanisms that contribute to its region-specific, neural progenitor cell-specific and temporal control.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 8","pages":"519-534"},"PeriodicalIF":28.7,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141477031","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 : 2024-07-01DOI: 10.1038/s41583-024-00841-x
Sian Lewis
The maladaptive reward learning associated with morphine administration is shown here to be mediated by changes in dopamine-release dynamics in reward circuitry resulting from increased myelination specifically in the ventral tegmental area.
{"title":"Wrapping up reward","authors":"Sian Lewis","doi":"10.1038/s41583-024-00841-x","DOIUrl":"10.1038/s41583-024-00841-x","url":null,"abstract":"The maladaptive reward learning associated with morphine administration is shown here to be mediated by changes in dopamine-release dynamics in reward circuitry resulting from increased myelination specifically in the ventral tegmental area.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 8","pages":"515-515"},"PeriodicalIF":28.7,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141477032","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 : 2024-07-01DOI: 10.1038/s41583-024-00843-9
Katherine Whalley
A study maps the effects of ageing and sex on gene regulation in specific human cortical cell types.
一项研究描绘了衰老和性别对特定人类皮质细胞类型基因调控的影响。
{"title":"Mapping the cell-type-specific effects of ageing in the human cortex","authors":"Katherine Whalley","doi":"10.1038/s41583-024-00843-9","DOIUrl":"10.1038/s41583-024-00843-9","url":null,"abstract":"A study maps the effects of ageing and sex on gene regulation in specific human cortical cell types.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 8","pages":"515-515"},"PeriodicalIF":28.7,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141489629","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 : 2024-06-27DOI: 10.1038/s41583-024-00836-8
Jacob A. Miller, Christos Constantinidis
The lateral prefrontal cortex (PFC) in humans and other primates is critical for immediate, goal-directed behaviour and working memory, which are classically considered distinct from the cognitive and neural circuits that support long-term learning and memory. Over the past few years, a reconsideration of this textbook perspective has emerged, in that different timescales of memory-guided behaviour are in constant interaction during the pursuit of immediate goals. Here, we will first detail how neural activity related to the shortest timescales of goal-directed behaviour (which requires maintenance of current states and goals in working memory) is sculpted by long-term knowledge and learning — that is, how the past informs present behaviour. Then, we will outline how learning across different timescales (from seconds to years) drives plasticity in the primate lateral PFC, from single neuron firing rates to mesoscale neuroimaging activity patterns. Finally, we will review how, over days and months of learning, dense local and long-range connectivity patterns in PFC facilitate longer-lasting changes in population activity by changing synaptic weights and recruiting additional neural resources to inform future behaviour. Our Review sheds light on how the machinery of plasticity in PFC circuits facilitates the integration of learned experiences across time to best guide adaptive behaviour. The prefrontal cortex is critical for working memory, over a timescale of seconds. In this Review, Miller and Constantinidis examine how the prefrontal cortex facilitates the integration of memory systems across other timescales as well. In this framework of prefrontal learning, short-term memory and long-term memory interact to serve goal-directed behaviour.
{"title":"Timescales of learning in prefrontal cortex","authors":"Jacob A. Miller, Christos Constantinidis","doi":"10.1038/s41583-024-00836-8","DOIUrl":"10.1038/s41583-024-00836-8","url":null,"abstract":"The lateral prefrontal cortex (PFC) in humans and other primates is critical for immediate, goal-directed behaviour and working memory, which are classically considered distinct from the cognitive and neural circuits that support long-term learning and memory. Over the past few years, a reconsideration of this textbook perspective has emerged, in that different timescales of memory-guided behaviour are in constant interaction during the pursuit of immediate goals. Here, we will first detail how neural activity related to the shortest timescales of goal-directed behaviour (which requires maintenance of current states and goals in working memory) is sculpted by long-term knowledge and learning — that is, how the past informs present behaviour. Then, we will outline how learning across different timescales (from seconds to years) drives plasticity in the primate lateral PFC, from single neuron firing rates to mesoscale neuroimaging activity patterns. Finally, we will review how, over days and months of learning, dense local and long-range connectivity patterns in PFC facilitate longer-lasting changes in population activity by changing synaptic weights and recruiting additional neural resources to inform future behaviour. Our Review sheds light on how the machinery of plasticity in PFC circuits facilitates the integration of learned experiences across time to best guide adaptive behaviour. The prefrontal cortex is critical for working memory, over a timescale of seconds. In this Review, Miller and Constantinidis examine how the prefrontal cortex facilitates the integration of memory systems across other timescales as well. In this framework of prefrontal learning, short-term memory and long-term memory interact to serve goal-directed behaviour.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 9","pages":"597-610"},"PeriodicalIF":28.7,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141461782","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 : 2024-06-27DOI: 10.1038/s41583-024-00830-0
David Williams
Bradykinesia, or slowness of movement, is a defining feature of Parkinson disease (PD) and a major contributor to the negative effects on quality of life associated with this disorder and related conditions. A dominant pathophysiological model of bradykinesia in PD has existed for approximately 30 years and has been the basis for the development of several therapeutic interventions, but accumulating evidence has made this model increasingly untenable. Although more recent models have been proposed, they also appear to be flawed. In this Perspective, I consider the leading prior models of bradykinesia in PD and argue that a more functionally related model is required, one that considers changes that disrupt the fundamental process of accurate information transmission. In doing so, I review emerging evidence of network level functional connectivity changes, information transfer dysfunction and potential motor code transmission error and present a novel model of bradykinesia in PD that incorporates this evidence. I hope that this model may reconcile inconsistencies in its predecessors and encourage further development of therapeutic interventions. There are a number of models that have attempted to explain why people with Parkinson disease move slowly. In this Perspective, Williams identifies the inconsistencies in these models and suggests that these may be addressed by a different model that considers disordered information transmission as fundamental to slow movement development.
{"title":"Why so slow? Models of parkinsonian bradykinesia","authors":"David Williams","doi":"10.1038/s41583-024-00830-0","DOIUrl":"10.1038/s41583-024-00830-0","url":null,"abstract":"Bradykinesia, or slowness of movement, is a defining feature of Parkinson disease (PD) and a major contributor to the negative effects on quality of life associated with this disorder and related conditions. A dominant pathophysiological model of bradykinesia in PD has existed for approximately 30 years and has been the basis for the development of several therapeutic interventions, but accumulating evidence has made this model increasingly untenable. Although more recent models have been proposed, they also appear to be flawed. In this Perspective, I consider the leading prior models of bradykinesia in PD and argue that a more functionally related model is required, one that considers changes that disrupt the fundamental process of accurate information transmission. In doing so, I review emerging evidence of network level functional connectivity changes, information transfer dysfunction and potential motor code transmission error and present a novel model of bradykinesia in PD that incorporates this evidence. I hope that this model may reconcile inconsistencies in its predecessors and encourage further development of therapeutic interventions. There are a number of models that have attempted to explain why people with Parkinson disease move slowly. In this Perspective, Williams identifies the inconsistencies in these models and suggests that these may be addressed by a different model that considers disordered information transmission as fundamental to slow movement development.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 8","pages":"573-586"},"PeriodicalIF":28.7,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141462375","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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