Pub Date : 2025-05-23DOI: 10.1038/s41583-025-00934-1
Sharif I. Kronemer, Peter A. Bandettini, Javier Gonzalez-Castillo
Consciousness is private. Although conscious beings directly access their own conscious experiences, the consciousness of others must be inferred through overt report: observable behaviours — such as overt facial expressions, vocalizations and body gestures — that suggest the level, state and content of consciousness. However, overt report is limited because it can be erroneous (for example, resulting from wilful deception or being subject to recall error), absent (for example, during sleep and paralysis) or conflict with research goals (for example, in no-report paradigms and resting-state studies). These limitations encourage the search for covert measures of consciousness: physiological signals that disclose consciousness without relying on overt behaviour. This Review highlights emerging covert measures of consciousness in humans, including eye, skin, respiratory and heart signals. We also address the challenge of distinguishing physiological signals linked to conscious versus unconscious neural processing. Finally, we consider the ethical implications of infringing on the innate privacy of consciousness. Consciousness may be inferred in others through observable behaviours such as facial expressions and vocalizations. However, such overt reporting has limitations, leading to research on physiological signals that disclose consciousness without relying on overt behaviour. In this Review, Kronemer, Bandettini and Gonzalez-Castillo explore such covert measures of consciousness in humans.
{"title":"Sleuthing subjectivity: a review of covert measures of consciousness","authors":"Sharif I. Kronemer, Peter A. Bandettini, Javier Gonzalez-Castillo","doi":"10.1038/s41583-025-00934-1","DOIUrl":"10.1038/s41583-025-00934-1","url":null,"abstract":"Consciousness is private. Although conscious beings directly access their own conscious experiences, the consciousness of others must be inferred through overt report: observable behaviours — such as overt facial expressions, vocalizations and body gestures — that suggest the level, state and content of consciousness. However, overt report is limited because it can be erroneous (for example, resulting from wilful deception or being subject to recall error), absent (for example, during sleep and paralysis) or conflict with research goals (for example, in no-report paradigms and resting-state studies). These limitations encourage the search for covert measures of consciousness: physiological signals that disclose consciousness without relying on overt behaviour. This Review highlights emerging covert measures of consciousness in humans, including eye, skin, respiratory and heart signals. We also address the challenge of distinguishing physiological signals linked to conscious versus unconscious neural processing. Finally, we consider the ethical implications of infringing on the innate privacy of consciousness. Consciousness may be inferred in others through observable behaviours such as facial expressions and vocalizations. However, such overt reporting has limitations, leading to research on physiological signals that disclose consciousness without relying on overt behaviour. In this Review, Kronemer, Bandettini and Gonzalez-Castillo explore such covert measures of consciousness in humans.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 8","pages":"476-496"},"PeriodicalIF":26.7,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144130170","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 : 2025-05-23DOI: 10.1038/s41583-025-00932-3
Ryosuke Tanaka (, ), Ruben Portugues
Despite the large evolutionary distance between vertebrates and insects, the visual systems of these two taxa bear remarkable similarities that have been noted repeatedly, including by pioneering neuroanatomists such as Ramón y Cajal. Fuelled by the advent of transgenic approaches in neuroscience, studies of visual system anatomy and function in both vertebrates and insects have made dramatic progress during the past two decades, revealing even deeper analogies between their visual systems than were noted by earlier observers. Such across-taxa comparisons have tended to focus on either elementary motion detection or relatively peripheral layers of the visual systems. By contrast, the aims of this Review are to expand the scope of this comparison to pathways outside visual motion detection, as well as to deeper visual structures. To achieve these aims, we primarily discuss examples from recent work in larval zebrafish (Danio rerio) and the fruitfly (Drosophila melanogaster), a pair of genetically tractable model organisms with comparatively sized, small brains. In particular, we argue that the brains of both vertebrates and insects are equipped with third-order visual structures that specialize in shared behavioural tasks, including postural and course stabilization, approach and avoidance, and some other behaviours. These wider analogies between the two distant taxa highlight shared behavioural goals and associated evolutionary constraints and suggest that studies on vertebrate and insect vision have a lot to inspire each other. The visual systems of vertebrates and insects exhibit considerable similarities. In this Review, Tanaka and Portugues discuss these similarities, focusing primarily on recent works in larval zebrafish and fruitflies and expanding the scope of the comparison from past examinations of this area.
尽管脊椎动物和昆虫之间的进化距离很远，但这两个分类群的视觉系统却有着惊人的相似之处，这一点已经被反复指出，包括神经解剖学先驱Ramón y Cajal在内。在神经科学中转基因方法的推动下，对脊椎动物和昆虫视觉系统解剖和功能的研究在过去二十年中取得了巨大进展，揭示了它们视觉系统之间比早期观察者所注意到的更深层次的相似之处。这种跨类群的比较往往集中在基本的运动检测或视觉系统的相对外围层。相比之下，本综述的目的是将这种比较的范围扩展到视觉运动检测之外的路径，以及更深层次的视觉结构。为了实现这些目标，我们主要讨论了最近在幼体斑马鱼（Danio rerio）和果蝇（Drosophila melanogaster）中研究的例子，这是一对遗传上易于处理的模式生物，它们的大脑相对较小。特别是，我们认为脊椎动物和昆虫的大脑都配备了三阶视觉结构，专门负责共同的行为任务，包括姿势和路线稳定，接近和回避，以及其他一些行为。这两个遥远的分类群之间的更广泛的相似性突出了共同的行为目标和相关的进化限制，并表明脊椎动物和昆虫视觉的研究有很多相互启发的地方。
{"title":"On analogies in vertebrate and insect visual systems","authors":"Ryosuke Tanaka \u0000 (, ), Ruben Portugues","doi":"10.1038/s41583-025-00932-3","DOIUrl":"10.1038/s41583-025-00932-3","url":null,"abstract":"Despite the large evolutionary distance between vertebrates and insects, the visual systems of these two taxa bear remarkable similarities that have been noted repeatedly, including by pioneering neuroanatomists such as Ramón y Cajal. Fuelled by the advent of transgenic approaches in neuroscience, studies of visual system anatomy and function in both vertebrates and insects have made dramatic progress during the past two decades, revealing even deeper analogies between their visual systems than were noted by earlier observers. Such across-taxa comparisons have tended to focus on either elementary motion detection or relatively peripheral layers of the visual systems. By contrast, the aims of this Review are to expand the scope of this comparison to pathways outside visual motion detection, as well as to deeper visual structures. To achieve these aims, we primarily discuss examples from recent work in larval zebrafish (Danio rerio) and the fruitfly (Drosophila melanogaster), a pair of genetically tractable model organisms with comparatively sized, small brains. In particular, we argue that the brains of both vertebrates and insects are equipped with third-order visual structures that specialize in shared behavioural tasks, including postural and course stabilization, approach and avoidance, and some other behaviours. These wider analogies between the two distant taxa highlight shared behavioural goals and associated evolutionary constraints and suggest that studies on vertebrate and insect vision have a lot to inspire each other. The visual systems of vertebrates and insects exhibit considerable similarities. In this Review, Tanaka and Portugues discuss these similarities, focusing primarily on recent works in larval zebrafish and fruitflies and expanding the scope of the comparison from past examinations of this area.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 8","pages":"456-475"},"PeriodicalIF":26.7,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144130169","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 : 2025-05-19DOI: 10.1038/s41583-025-00930-5
Peng Lei, Tara Walker, Scott Ayton
Ferroptosis is a type of cell death process defined by iron-dependent peroxidation of phospholipids leading to the destruction of cellular membranes and death of the cell. Ferroptosis occurs throughout the body, but a considerable research focus on ferroptosis in the brain — neuroferroptosis — has been driven by the rich lipid and iron content of the brain as well as its high oxygen consumption. Neurons also have an exceptionally large surface area and metabolic demand, which necessitates specific mechanisms (such as lipid antioxidants) to engage constantly to protect the plasma membrane against lipid peroxidation. Ferroptosis has been extensively linked to neurodegeneration and ischaemia and is increasingly implicated in physiological processes such as neuronal reprogramming. Astrocytes provide metabolic support to neurons, enabling them to defend against ferroptosis, yet ferroptotic signals in microglia can propagate damage to astrocytes and neurons, highlighting the complex intercellular (patho)physiology of neuroferroptosis. The brain’s high lipid content, iron levels and oxygen metabolism uniquely predispose it to ferroptosis, an iron-dependent form of regulated cell death. In this Review, Lei et al. discuss brain-specific vulnerabilities and the physiological and pathological implications of neuroferroptosis.
{"title":"Neuroferroptosis in health and diseases","authors":"Peng Lei, Tara Walker, Scott Ayton","doi":"10.1038/s41583-025-00930-5","DOIUrl":"10.1038/s41583-025-00930-5","url":null,"abstract":"Ferroptosis is a type of cell death process defined by iron-dependent peroxidation of phospholipids leading to the destruction of cellular membranes and death of the cell. Ferroptosis occurs throughout the body, but a considerable research focus on ferroptosis in the brain — neuroferroptosis — has been driven by the rich lipid and iron content of the brain as well as its high oxygen consumption. Neurons also have an exceptionally large surface area and metabolic demand, which necessitates specific mechanisms (such as lipid antioxidants) to engage constantly to protect the plasma membrane against lipid peroxidation. Ferroptosis has been extensively linked to neurodegeneration and ischaemia and is increasingly implicated in physiological processes such as neuronal reprogramming. Astrocytes provide metabolic support to neurons, enabling them to defend against ferroptosis, yet ferroptotic signals in microglia can propagate damage to astrocytes and neurons, highlighting the complex intercellular (patho)physiology of neuroferroptosis. The brain’s high lipid content, iron levels and oxygen metabolism uniquely predispose it to ferroptosis, an iron-dependent form of regulated cell death. In this Review, Lei et al. discuss brain-specific vulnerabilities and the physiological and pathological implications of neuroferroptosis.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 8","pages":"497-511"},"PeriodicalIF":26.7,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144087867","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 : 2025-05-16DOI: 10.1038/s41583-025-00933-2
Melissa L. Perreault, Rudi Taylor-Bragge, Hervé Chneiweiss, Andre D. McLachlan, T. Ryan Gregory, Roksana Khalid, Katherine Bassil, Anna Lydia Svalastog, Minerva R. Velarde, Judy Illes
Despite a global push to recognize Indigenous knowledge systems in research, neuroscience remains embedded in Euro-Western ways of means and methods. Authentic capacity-building will bring Indigenous ways of knowing and doing to the neuroscience workforce, to research and to training, and will lead to diversified and strengthened approaches to discovery and clinical care strategies.
{"title":"Indigenous representation in neuroscience scholarship, teaching and care","authors":"Melissa L. Perreault, Rudi Taylor-Bragge, Hervé Chneiweiss, Andre D. McLachlan, T. Ryan Gregory, Roksana Khalid, Katherine Bassil, Anna Lydia Svalastog, Minerva R. Velarde, Judy Illes","doi":"10.1038/s41583-025-00933-2","DOIUrl":"10.1038/s41583-025-00933-2","url":null,"abstract":"Despite a global push to recognize Indigenous knowledge systems in research, neuroscience remains embedded in Euro-Western ways of means and methods. Authentic capacity-building will bring Indigenous ways of knowing and doing to the neuroscience workforce, to research and to training, and will lead to diversified and strengthened approaches to discovery and clinical care strategies.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 7","pages":"373-375"},"PeriodicalIF":26.7,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144065972","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 : 2025-05-16DOI: 10.1038/s41583-025-00929-y
Michael C. Anderson, Maite Crespo-Garcia, S. Subbulakshmi
Controlling action and thought requires the capacity to stop mental processes. Over the past two decades, evidence has grown that a domain-general inhibitory control mechanism supported by the right lateral prefrontal cortex achieves these functions. However, current views of the neural mechanisms of inhibitory control derive largely from research into the stopping of action. Whereas action stopping is a convenient empirical model, it does not invoke thought inhibition and cannot be used to identify the unique features of this process. Here, we review research that addresses how organisms stop a key process that drives thoughts: memory retrieval. This work has shown that retrieval stopping shares right dorsolateral and ventrolateral prefrontal mechanisms with action stopping, consistent with a domain-general inhibitory control mechanism, but also recruits a distinct fronto-temporal pathway that determines the success of mental control. As part of this pathway, GABAergic inhibition within the hippocampus influences the efficacy of prefrontal control over thought. These unique elements of mental control suggest that hippocampal disinhibition is a transdiagnostic factor underlying intrusive thinking, linking the fronto-temporal control pathway to preclinical models of psychiatric disorders and fear extinction. We suggest that retrieval-stopping deficits may underlie the intrusive thinking that is common across many psychiatric disorders. The capacity to prevent unwanted thoughts is important for cognitive function and mental health. Anderson et al. describe insights into the neural mechanisms of the inhibitory control of thought that have been gained from studies of retrieval stopping and discuss how this knowledge informs our understanding of psychiatric disorders associated with intrusive thinking.
{"title":"Brain mechanisms underlying the inhibitory control of thought","authors":"Michael C. Anderson, Maite Crespo-Garcia, S. Subbulakshmi","doi":"10.1038/s41583-025-00929-y","DOIUrl":"10.1038/s41583-025-00929-y","url":null,"abstract":"Controlling action and thought requires the capacity to stop mental processes. Over the past two decades, evidence has grown that a domain-general inhibitory control mechanism supported by the right lateral prefrontal cortex achieves these functions. However, current views of the neural mechanisms of inhibitory control derive largely from research into the stopping of action. Whereas action stopping is a convenient empirical model, it does not invoke thought inhibition and cannot be used to identify the unique features of this process. Here, we review research that addresses how organisms stop a key process that drives thoughts: memory retrieval. This work has shown that retrieval stopping shares right dorsolateral and ventrolateral prefrontal mechanisms with action stopping, consistent with a domain-general inhibitory control mechanism, but also recruits a distinct fronto-temporal pathway that determines the success of mental control. As part of this pathway, GABAergic inhibition within the hippocampus influences the efficacy of prefrontal control over thought. These unique elements of mental control suggest that hippocampal disinhibition is a transdiagnostic factor underlying intrusive thinking, linking the fronto-temporal control pathway to preclinical models of psychiatric disorders and fear extinction. We suggest that retrieval-stopping deficits may underlie the intrusive thinking that is common across many psychiatric disorders. The capacity to prevent unwanted thoughts is important for cognitive function and mental health. Anderson et al. describe insights into the neural mechanisms of the inhibitory control of thought that have been gained from studies of retrieval stopping and discuss how this knowledge informs our understanding of psychiatric disorders associated with intrusive thinking.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 7","pages":"415-437"},"PeriodicalIF":26.7,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144067138","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 : 2025-05-13DOI: 10.1038/s41583-025-00926-1
Yi Liu, Troy W. Whitfield, George W. Bell, Ruisi Guo, Anthony Flamier, Richard A. Young, Rudolf Jaenisch
Rett syndrome (RTT) is a neurodevelopmental disorder that is mainly caused by mutations in the methyl-DNA-binding protein MECP2. MECP2 is an important epigenetic regulator that plays a pivotal role in neuronal gene regulation, where it has been reported to function as both a repressor and an activator. Despite extensive efforts in mechanistic studies over the past two decades, a clear consensus on how MECP2 dysfunction impacts molecular mechanisms and contributes to disease progression has not been reached. Here, we review recent insights from epigenomic, transcriptomic and proteomic studies that advance our understanding of MECP2 as an interacting hub for DNA, RNA and transcription factors, orchestrating diverse processes that are crucial for neuronal function. By discussing findings from different model systems, we identify crucial epigenetic details and cofactor interactions, enriching our understanding of the multifaceted roles of MECP2 in transcriptional regulation and chromatin structure. These mechanistic insights offer potential avenues for rational therapeutic design for RTT. Mutations in the gene encoding the methyl-DNA-binding protein MECP2 cause Rett syndrome. Jaenisch and colleagues here provide an overview of our current understanding of the mechanisms by which MECP2 interacts with DNA and its diverse roles in gene regulation, and consider the implications of these insights for future therapeutic interventions.
{"title":"Exploring the complexity of MECP2 function in Rett syndrome","authors":"Yi Liu, Troy W. Whitfield, George W. Bell, Ruisi Guo, Anthony Flamier, Richard A. Young, Rudolf Jaenisch","doi":"10.1038/s41583-025-00926-1","DOIUrl":"10.1038/s41583-025-00926-1","url":null,"abstract":"Rett syndrome (RTT) is a neurodevelopmental disorder that is mainly caused by mutations in the methyl-DNA-binding protein MECP2. MECP2 is an important epigenetic regulator that plays a pivotal role in neuronal gene regulation, where it has been reported to function as both a repressor and an activator. Despite extensive efforts in mechanistic studies over the past two decades, a clear consensus on how MECP2 dysfunction impacts molecular mechanisms and contributes to disease progression has not been reached. Here, we review recent insights from epigenomic, transcriptomic and proteomic studies that advance our understanding of MECP2 as an interacting hub for DNA, RNA and transcription factors, orchestrating diverse processes that are crucial for neuronal function. By discussing findings from different model systems, we identify crucial epigenetic details and cofactor interactions, enriching our understanding of the multifaceted roles of MECP2 in transcriptional regulation and chromatin structure. These mechanistic insights offer potential avenues for rational therapeutic design for RTT. Mutations in the gene encoding the methyl-DNA-binding protein MECP2 cause Rett syndrome. Jaenisch and colleagues here provide an overview of our current understanding of the mechanisms by which MECP2 interacts with DNA and its diverse roles in gene regulation, and consider the implications of these insights for future therapeutic interventions.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 7","pages":"379-398"},"PeriodicalIF":26.7,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143939978","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 : 2025-05-07DOI: 10.1038/s41583-025-00928-z
Sian Lewis
A possible mechanism for the increased incidence of mood disorders in people with immune system disorders such as psoriasis is revealed where, in mice, elevated serum levels of the cytokines IL-17A and IL-17C induce anxiety-like symptoms via activation of neurons in the anterior basolateral amygdala.
{"title":"Getting anxious about immune system activation","authors":"Sian Lewis","doi":"10.1038/s41583-025-00928-z","DOIUrl":"10.1038/s41583-025-00928-z","url":null,"abstract":"A possible mechanism for the increased incidence of mood disorders in people with immune system disorders such as psoriasis is revealed where, in mice, elevated serum levels of the cytokines IL-17A and IL-17C induce anxiety-like symptoms via activation of neurons in the anterior basolateral amygdala.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 6","pages":"310-310"},"PeriodicalIF":26.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143915674","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 : 2025-05-07DOI: 10.1038/s41583-025-00925-2
Jaeeon Lee, Bernardo L. Sabatini
A hallmark of optimal reinforcement learning is that an agent learns to avoid actions that lead to negative outcomes while still exploring alternative actions that could lead to better outcomes. Although the basal ganglia have been hypothesized to contribute to this computation, the mechanisms by which they do so are still unclear. Here, we focus on the function of the striatal indirect pathway and propose that it is regulated by a synaptic plasticity rule that allows an animal to avoid actions that lead to suboptimal outcomes. We consider current theories of striatal indirect pathway function in light of recent experimental findings and discuss studies that suggest that indirect pathway activity is potentiated by the suppression of dopamine release in the striatum. Furthermore, we highlight recent studies showing that activation of the indirect pathway can trigger an action, allowing animals to explore new actions while suppressing suboptimal actions. We show how our framework can reconcile previously conflicting results regarding the indirect pathway and suggest experiments for future investigation. The functional roles of the striatal indirect pathway remain unclear. In this Perspective, Lee and Sabatini propose that a three-factor learning rule governs the activity of indirect striatal projection neurons, contributing to the learnt avoidance of actions with negative outcomes and the transition to alternative actions.
{"title":"From avoidance to new action: the multifaceted role of the striatal indirect pathway","authors":"Jaeeon Lee, Bernardo L. Sabatini","doi":"10.1038/s41583-025-00925-2","DOIUrl":"10.1038/s41583-025-00925-2","url":null,"abstract":"A hallmark of optimal reinforcement learning is that an agent learns to avoid actions that lead to negative outcomes while still exploring alternative actions that could lead to better outcomes. Although the basal ganglia have been hypothesized to contribute to this computation, the mechanisms by which they do so are still unclear. Here, we focus on the function of the striatal indirect pathway and propose that it is regulated by a synaptic plasticity rule that allows an animal to avoid actions that lead to suboptimal outcomes. We consider current theories of striatal indirect pathway function in light of recent experimental findings and discuss studies that suggest that indirect pathway activity is potentiated by the suppression of dopamine release in the striatum. Furthermore, we highlight recent studies showing that activation of the indirect pathway can trigger an action, allowing animals to explore new actions while suppressing suboptimal actions. We show how our framework can reconcile previously conflicting results regarding the indirect pathway and suggest experiments for future investigation. The functional roles of the striatal indirect pathway remain unclear. In this Perspective, Lee and Sabatini propose that a three-factor learning rule governs the activity of indirect striatal projection neurons, contributing to the learnt avoidance of actions with negative outcomes and the transition to alternative actions.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 7","pages":"438-449"},"PeriodicalIF":26.7,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143920271","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 : 2025-05-06DOI: 10.1038/s41583-025-00931-4
Darran Yates
A new study reveals over 40 functionally different types of amacrine cell in the mouse retina.
一项新的研究揭示了小鼠视网膜中40多种功能不同的无分泌细胞。
{"title":"Functional diversity of amacrine cells","authors":"Darran Yates","doi":"10.1038/s41583-025-00931-4","DOIUrl":"10.1038/s41583-025-00931-4","url":null,"abstract":"A new study reveals over 40 functionally different types of amacrine cell in the mouse retina.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"26 6","pages":"309-309"},"PeriodicalIF":26.7,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143910506","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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