Pub Date : 2024-08-06DOI: 10.1038/s41593-024-01696-2
Alexander L. Tesmer, Xinyang Li, Eva Bracey, Cyra Schmandt, Rafael Polania, Daria Peleg-Raibstein, Denis Burdakov
Despite the well-known health benefits of physical activity, many people underexercise; what drives the prioritization of exercise over alternative options is unclear. We developed a task that enabled us to study how mice freely and rapidly alternate between wheel running and other voluntary activities, such as eating palatable food. When multiple alternatives were available, mice chose to spend a substantial amount of time wheel running without any extrinsic reward and maintained this behavior even when palatable food was added as an option. Causal manipulations and correlative analyses of appetitive and consummatory processes revealed this preference for wheel running to be instantiated by hypothalamic hypocretin/orexin neurons (HONs). The effect of HON manipulations on wheel running and eating was strongly context-dependent, being the largest in the scenario where both options were available. Overall, these data suggest that HON activity enables an eat–run arbitration that results in choosing exercise over food. What makes the brain maintain voluntary exercise despite attractive alternative options such as eating? Tesmer et al. show that orexin/hypocretin neurons are crucial for implementing the underlying valuation of eating versus running in mice.
{"title":"Orexin neurons mediate temptation-resistant voluntary exercise","authors":"Alexander L. Tesmer, Xinyang Li, Eva Bracey, Cyra Schmandt, Rafael Polania, Daria Peleg-Raibstein, Denis Burdakov","doi":"10.1038/s41593-024-01696-2","DOIUrl":"10.1038/s41593-024-01696-2","url":null,"abstract":"Despite the well-known health benefits of physical activity, many people underexercise; what drives the prioritization of exercise over alternative options is unclear. We developed a task that enabled us to study how mice freely and rapidly alternate between wheel running and other voluntary activities, such as eating palatable food. When multiple alternatives were available, mice chose to spend a substantial amount of time wheel running without any extrinsic reward and maintained this behavior even when palatable food was added as an option. Causal manipulations and correlative analyses of appetitive and consummatory processes revealed this preference for wheel running to be instantiated by hypothalamic hypocretin/orexin neurons (HONs). The effect of HON manipulations on wheel running and eating was strongly context-dependent, being the largest in the scenario where both options were available. Overall, these data suggest that HON activity enables an eat–run arbitration that results in choosing exercise over food. What makes the brain maintain voluntary exercise despite attractive alternative options such as eating? Tesmer et al. show that orexin/hypocretin neurons are crucial for implementing the underlying valuation of eating versus running in mice.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":null,"pages":null},"PeriodicalIF":21.2,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41593-024-01696-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141895363","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 : 2024-08-06DOI: 10.1038/s41593-024-01735-y
In this special issue of Nature Neuroscience, we shine a spotlight on glia. Research into glia has become one of the most exciting and dynamic subfields of neuroscience, yet there is still much to be discovered about the diverse forms and functions of these cells.
{"title":"Glia move to the foreground","authors":"","doi":"10.1038/s41593-024-01735-y","DOIUrl":"10.1038/s41593-024-01735-y","url":null,"abstract":"In this special issue of Nature Neuroscience, we shine a spotlight on glia. Research into glia has become one of the most exciting and dynamic subfields of neuroscience, yet there is still much to be discovered about the diverse forms and functions of these cells.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":null,"pages":null},"PeriodicalIF":21.2,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41593-024-01735-y.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141897884","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 : 2024-08-06DOI: 10.1038/s41593-024-01717-0
Shari Wiseman
As part of our special issue focused on glia, we are having conversations with both established leaders in the field and those earlier in their careers to discuss how the field has evolved and where it is heading. Here, we speak with Beth Stevens, Associate Professor of Neurology at the F. M. Kirby Neurobiology Center at Boston Children’s Hospital and at the Broad Institute of MIT and Harvard. We spoke about how she initially became fascinated with glia, her work to understand how glia interact with synapses, and the technologies that are needed to usher in the next era of discoveries in the field.
作为以神经胶质细胞为主题的特刊的一部分，我们将与该领域的资深领军人物和处于职业生涯早期的人士进行对话，讨论该领域的发展历程和未来方向。在这里，我们采访了波士顿儿童医院科比神经生物学中心（F. M. Kirby Neurobiology Center）以及麻省理工学院和哈佛大学布罗德研究所（Broad Institute of MIT and Harvard）的神经学副教授贝丝-史蒂文斯（Beth Stevens）。我们谈到了她最初是如何对神经胶质细胞着迷的、她为了解神经胶质细胞如何与突触相互作用所做的工作，以及该领域迎来下一个发现时代所需的技术。
{"title":"In conversation with Beth Stevens","authors":"Shari Wiseman","doi":"10.1038/s41593-024-01717-0","DOIUrl":"10.1038/s41593-024-01717-0","url":null,"abstract":"As part of our special issue focused on glia, we are having conversations with both established leaders in the field and those earlier in their careers to discuss how the field has evolved and where it is heading. Here, we speak with Beth Stevens, Associate Professor of Neurology at the F. M. Kirby Neurobiology Center at Boston Children’s Hospital and at the Broad Institute of MIT and Harvard. We spoke about how she initially became fascinated with glia, her work to understand how glia interact with synapses, and the technologies that are needed to usher in the next era of discoveries in the field.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":null,"pages":null},"PeriodicalIF":21.2,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141897886","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 : 2024-08-05DOI: 10.1038/s41593-024-01730-3
Andrew Octavian Sasmita, Constanze Depp, Taisiia Nazarenko, Ting Sun, Sophie B. Siems, Erinne Cherisse Ong, Yakum B. Nkeh, Carolin Böhler, Xuan Yu, Bastian Bues, Lisa Evangelista, Shuying Mao, Barbara Morgado, Zoe Wu, Torben Ruhwedel, Swati Subramanian, Friederike Börensen, Katharina Overhoff, Lena Spieth, Stefan A. Berghoff, Katherine Rose Sadleir, Robert Vassar, Simone Eggert, Sandra Goebbels, Takashi Saito, Takaomi Saido, Gesine Saher, Wiebke Möbius, Gonçalo Castelo-Branco, Hans-Wolfgang Klafki, Oliver Wirths, Jens Wiltfang, Sarah Jäkel, Riqiang Yan, Klaus-Armin Nave
Amyloid-β (Aβ) is thought to be neuronally derived in Alzheimer’s disease (AD). However, transcripts of amyloid precursor protein (APP) and amyloidogenic enzymes are equally abundant in oligodendrocytes (OLs). By cell-type-specific deletion of Bace1 in a humanized knock-in AD model, APPNLGF, we demonstrate that OLs and neurons contribute to Aβ plaque burden. For rapid plaque seeding, excitatory projection neurons must provide a threshold level of Aβ. Ultimately, our findings are relevant for AD prevention and therapeutic strategies. In Alzheimer’s disease, neurons are considered the sole source of amyloid-β (Aβ) peptides that form plaques. Here the authors show that oligodendrocytes, the myelinating glial cells of the brain, also contribute to Aβ plaque burden alongside neurons.
{"title":"Oligodendrocytes produce amyloid-β and contribute to plaque formation alongside neurons in Alzheimer’s disease model mice","authors":"Andrew Octavian Sasmita, Constanze Depp, Taisiia Nazarenko, Ting Sun, Sophie B. Siems, Erinne Cherisse Ong, Yakum B. Nkeh, Carolin Böhler, Xuan Yu, Bastian Bues, Lisa Evangelista, Shuying Mao, Barbara Morgado, Zoe Wu, Torben Ruhwedel, Swati Subramanian, Friederike Börensen, Katharina Overhoff, Lena Spieth, Stefan A. Berghoff, Katherine Rose Sadleir, Robert Vassar, Simone Eggert, Sandra Goebbels, Takashi Saito, Takaomi Saido, Gesine Saher, Wiebke Möbius, Gonçalo Castelo-Branco, Hans-Wolfgang Klafki, Oliver Wirths, Jens Wiltfang, Sarah Jäkel, Riqiang Yan, Klaus-Armin Nave","doi":"10.1038/s41593-024-01730-3","DOIUrl":"10.1038/s41593-024-01730-3","url":null,"abstract":"Amyloid-β (Aβ) is thought to be neuronally derived in Alzheimer’s disease (AD). However, transcripts of amyloid precursor protein (APP) and amyloidogenic enzymes are equally abundant in oligodendrocytes (OLs). By cell-type-specific deletion of Bace1 in a humanized knock-in AD model, APPNLGF, we demonstrate that OLs and neurons contribute to Aβ plaque burden. For rapid plaque seeding, excitatory projection neurons must provide a threshold level of Aβ. Ultimately, our findings are relevant for AD prevention and therapeutic strategies. In Alzheimer’s disease, neurons are considered the sole source of amyloid-β (Aβ) peptides that form plaques. Here the authors show that oligodendrocytes, the myelinating glial cells of the brain, also contribute to Aβ plaque burden alongside neurons.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":null,"pages":null},"PeriodicalIF":21.2,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41593-024-01730-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141891858","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 : 2024-08-05DOI: 10.1038/s41593-024-01726-z
Lizheng Wang, Qianqian Guo, Sandesh Acharya, Xiao Zheng, Vanessa Huynh, Brandon Whitmore, Askar Yimit, Mehr Malhotra, Siddharth Chatterji, Nicole Rosin, Elodie Labit, Colten Chipak, Kelsea Gorzo, Jordan Haidey, David A. Elliott, Tina Ram, Qingrun Zhang, Hedwich Kuipers, Grant Gordon, Jeff Biernaskie, Jiami Guo
Astrocyte diversity is greatly influenced by local environmental modulation. Here we report that the majority of astrocytes across the mouse brain possess a singular primary cilium localized to the cell soma. Comparative single-cell transcriptomics reveals that primary cilia mediate canonical SHH signaling to modulate astrocyte subtype-specific core features in synaptic regulation, intracellular transport, energy and metabolism. Independent of canonical SHH signaling, primary cilia are important regulators of astrocyte morphology and intracellular signaling balance. Dendritic spine analysis and transcriptomics reveal that perturbation of astrocytic cilia leads to disruption of neuronal development and global intercellular connectomes in the brain. Mice with primary ciliary-deficient astrocytes show behavioral deficits in sensorimotor function, sociability, learning and memory. Our results uncover a critical role for primary cilia in transmitting local cues that drive the region-specific diversification of astrocytes within the developing brain. Astrocyte diversity is greatly influenced by local environmental modulation. Wang et al. report a critical role for astrocytic primary cilia in transmitting local cues that drive the region-specific diversification of astrocytes within the developing mouse brain.
{"title":"Primary cilia signaling in astrocytes mediates development and regional-specific functional specification","authors":"Lizheng Wang, Qianqian Guo, Sandesh Acharya, Xiao Zheng, Vanessa Huynh, Brandon Whitmore, Askar Yimit, Mehr Malhotra, Siddharth Chatterji, Nicole Rosin, Elodie Labit, Colten Chipak, Kelsea Gorzo, Jordan Haidey, David A. Elliott, Tina Ram, Qingrun Zhang, Hedwich Kuipers, Grant Gordon, Jeff Biernaskie, Jiami Guo","doi":"10.1038/s41593-024-01726-z","DOIUrl":"10.1038/s41593-024-01726-z","url":null,"abstract":"Astrocyte diversity is greatly influenced by local environmental modulation. Here we report that the majority of astrocytes across the mouse brain possess a singular primary cilium localized to the cell soma. Comparative single-cell transcriptomics reveals that primary cilia mediate canonical SHH signaling to modulate astrocyte subtype-specific core features in synaptic regulation, intracellular transport, energy and metabolism. Independent of canonical SHH signaling, primary cilia are important regulators of astrocyte morphology and intracellular signaling balance. Dendritic spine analysis and transcriptomics reveal that perturbation of astrocytic cilia leads to disruption of neuronal development and global intercellular connectomes in the brain. Mice with primary ciliary-deficient astrocytes show behavioral deficits in sensorimotor function, sociability, learning and memory. Our results uncover a critical role for primary cilia in transmitting local cues that drive the region-specific diversification of astrocytes within the developing brain. Astrocyte diversity is greatly influenced by local environmental modulation. Wang et al. report a critical role for astrocytic primary cilia in transmitting local cues that drive the region-specific diversification of astrocytes within the developing mouse brain.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":null,"pages":null},"PeriodicalIF":21.2,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141891861","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 : 2024-08-05DOI: 10.1038/s41593-024-01728-x
Callista Yee, Yutong Xiao, Hongwen Chen, Anay R. Reddy, Bing Xu, Taylor N. Medwig-Kinney, Wan Zhang, Alan P. Boyle, Wendy A. Herbst, Yang Kevin Xiang, David Q. Matus, Kang Shen
Although the molecular composition and architecture of synapses have been widely explored, much less is known about what genetic programs directly activate synaptic gene expression and how they are modulated. Here, using Caenorhabditis elegans dopaminergic neurons, we reveal that EGL-43/MECOM and FOS-1/FOS control an activity-dependent synaptogenesis program. Loss of either factor severely reduces presynaptic protein expression. Both factors bind directly to promoters of synaptic genes and act together with CUT homeobox transcription factors to activate transcription. egl-43 and fos-1 mutually promote each other’s expression, and increasing the binding affinity of FOS-1 to the egl-43 locus results in increased presynaptic protein expression and synaptic function. EGL-43 regulates the expression of multiple transcription factors, including activity-regulated factors and developmental factors that define multiple aspects of dopaminergic identity. Together, we describe a robust genetic program underlying activity-regulated synapse formation during development. Neuronal activity contributes to synapse formation and plasticity. Here the authors demonstrate that activity stimulates developmental programs to directly modulate synapse formation.
{"title":"An activity-regulated transcriptional program directly drives synaptogenesis","authors":"Callista Yee, Yutong Xiao, Hongwen Chen, Anay R. Reddy, Bing Xu, Taylor N. Medwig-Kinney, Wan Zhang, Alan P. Boyle, Wendy A. Herbst, Yang Kevin Xiang, David Q. Matus, Kang Shen","doi":"10.1038/s41593-024-01728-x","DOIUrl":"10.1038/s41593-024-01728-x","url":null,"abstract":"Although the molecular composition and architecture of synapses have been widely explored, much less is known about what genetic programs directly activate synaptic gene expression and how they are modulated. Here, using Caenorhabditis elegans dopaminergic neurons, we reveal that EGL-43/MECOM and FOS-1/FOS control an activity-dependent synaptogenesis program. Loss of either factor severely reduces presynaptic protein expression. Both factors bind directly to promoters of synaptic genes and act together with CUT homeobox transcription factors to activate transcription. egl-43 and fos-1 mutually promote each other’s expression, and increasing the binding affinity of FOS-1 to the egl-43 locus results in increased presynaptic protein expression and synaptic function. EGL-43 regulates the expression of multiple transcription factors, including activity-regulated factors and developmental factors that define multiple aspects of dopaminergic identity. Together, we describe a robust genetic program underlying activity-regulated synapse formation during development. Neuronal activity contributes to synapse formation and plasticity. Here the authors demonstrate that activity stimulates developmental programs to directly modulate synapse formation.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":null,"pages":null},"PeriodicalIF":21.2,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41593-024-01728-x.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141891862","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 : 2024-08-02DOI: 10.1038/s41593-024-01724-1
Laurine Decoster, Sara Trova, Stefano Zucca, Janice Bulk, Ayden Gouveia, Gaetan Ternier, Tori Lhomme, Amandine Legrand, Sarah Gallet, Ulrich Boehm, Amanda Wyatt, Vanessa Wahl, Philipp Wartenberg, Erik Hrabovszky, Gergely Rácz, Federico Luzzati, Giulia Nato, Marco Fogli, Paolo Peretto, Sonja C. Schriever, Miriam Bernecker, Paul T. Pfluger, Sophie M. Steculorum, Serena Bovetti, Sowmyalakshmi Rasika, Vincent Prevot, Mauro S. B. Silva, Paolo Giacobini
Hypothalamic gonadotropin-releasing hormone (GnRH) neurons regulate fertility and integrate hormonal status with environmental cues to ensure reproductive success. Here we show that GnRH neurons in the olfactory bulb (GnRHOB) of adult mice can mediate social recognition. Specifically, we show that GnRHOB neurons extend neurites into the vomeronasal organ and olfactory epithelium and project to the median eminence. GnRHOB neurons in males express vomeronasal and olfactory receptors, are activated by female odors and mediate gonadotropin release in response to female urine. Male preference for female odors required the presence and activation of GnRHOB neurons, was impaired after genetic inhibition or ablation of these cells and relied on GnRH signaling in the posterodorsal medial amygdala. GnRH receptor expression in amygdala kisspeptin neurons appear to be required for GnRHOB neurons’ actions on male mounting behavior. Taken together, these results establish GnRHOB neurons as regulating fertility, sex recognition and mating in male mice. Studying GnRH neuroendocrine cells in the mouse olfactory bulb (GnRHOB neurons), Decoster et al. show that these cells respond to female odors and their activation regulates males’ female-odor preference and mating behavior.
{"title":"A GnRH neuronal population in the olfactory bulb translates socially relevant odors into reproductive behavior in male mice","authors":"Laurine Decoster, Sara Trova, Stefano Zucca, Janice Bulk, Ayden Gouveia, Gaetan Ternier, Tori Lhomme, Amandine Legrand, Sarah Gallet, Ulrich Boehm, Amanda Wyatt, Vanessa Wahl, Philipp Wartenberg, Erik Hrabovszky, Gergely Rácz, Federico Luzzati, Giulia Nato, Marco Fogli, Paolo Peretto, Sonja C. Schriever, Miriam Bernecker, Paul T. Pfluger, Sophie M. Steculorum, Serena Bovetti, Sowmyalakshmi Rasika, Vincent Prevot, Mauro S. B. Silva, Paolo Giacobini","doi":"10.1038/s41593-024-01724-1","DOIUrl":"10.1038/s41593-024-01724-1","url":null,"abstract":"Hypothalamic gonadotropin-releasing hormone (GnRH) neurons regulate fertility and integrate hormonal status with environmental cues to ensure reproductive success. Here we show that GnRH neurons in the olfactory bulb (GnRHOB) of adult mice can mediate social recognition. Specifically, we show that GnRHOB neurons extend neurites into the vomeronasal organ and olfactory epithelium and project to the median eminence. GnRHOB neurons in males express vomeronasal and olfactory receptors, are activated by female odors and mediate gonadotropin release in response to female urine. Male preference for female odors required the presence and activation of GnRHOB neurons, was impaired after genetic inhibition or ablation of these cells and relied on GnRH signaling in the posterodorsal medial amygdala. GnRH receptor expression in amygdala kisspeptin neurons appear to be required for GnRHOB neurons’ actions on male mounting behavior. Taken together, these results establish GnRHOB neurons as regulating fertility, sex recognition and mating in male mice. Studying GnRH neuroendocrine cells in the mouse olfactory bulb (GnRHOB neurons), Decoster et al. show that these cells respond to female odors and their activation regulates males’ female-odor preference and mating behavior.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":null,"pages":null},"PeriodicalIF":21.2,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141877414","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 : 2024-07-29DOI: 10.1038/s41593-024-01704-5
Benjamin Ehret, Roman Boehringer, Elizabeth A. Amadei, Maria R. Cervera, Christian Henning, Aniruddh R. Galgali, Valerio Mante, Benjamin F. Grewe
The medial prefrontal cortex (mPFC) has been proposed to link sensory inputs and behavioral outputs to mediate the execution of learned behaviors. However, how such a link is implemented has remained unclear. To measure prefrontal neural correlates of sensory stimuli and learned behaviors, we performed population calcium imaging during a new tone-signaled active avoidance paradigm in mice. We developed an analysis approach based on dimensionality reduction and decoding that allowed us to identify interpretable task-related population activity patterns. While a large fraction of tone-evoked activity was not informative about behavior execution, we identified an activity pattern that was predictive of tone-induced avoidance actions and did not occur for spontaneous actions with similar motion kinematics. Moreover, this avoidance-specific activity differed between distinct avoidance actions learned in two consecutive tasks. Overall, our results are consistent with a model in which mPFC contributes to the selection of goal-directed actions by transforming sensory inputs into specific behavioral outputs through distributed population-level computations. Ehret et al. uncover neural activity patterns in the prefrontal cortex that link sensory stimuli to learned behavioral responses by isolating interpretable activity patterns that are shared among mice performing the same task.
{"title":"Population-level coding of avoidance learning in medial prefrontal cortex","authors":"Benjamin Ehret, Roman Boehringer, Elizabeth A. Amadei, Maria R. Cervera, Christian Henning, Aniruddh R. Galgali, Valerio Mante, Benjamin F. Grewe","doi":"10.1038/s41593-024-01704-5","DOIUrl":"10.1038/s41593-024-01704-5","url":null,"abstract":"The medial prefrontal cortex (mPFC) has been proposed to link sensory inputs and behavioral outputs to mediate the execution of learned behaviors. However, how such a link is implemented has remained unclear. To measure prefrontal neural correlates of sensory stimuli and learned behaviors, we performed population calcium imaging during a new tone-signaled active avoidance paradigm in mice. We developed an analysis approach based on dimensionality reduction and decoding that allowed us to identify interpretable task-related population activity patterns. While a large fraction of tone-evoked activity was not informative about behavior execution, we identified an activity pattern that was predictive of tone-induced avoidance actions and did not occur for spontaneous actions with similar motion kinematics. Moreover, this avoidance-specific activity differed between distinct avoidance actions learned in two consecutive tasks. Overall, our results are consistent with a model in which mPFC contributes to the selection of goal-directed actions by transforming sensory inputs into specific behavioral outputs through distributed population-level computations. Ehret et al. uncover neural activity patterns in the prefrontal cortex that link sensory stimuli to learned behavioral responses by isolating interpretable activity patterns that are shared among mice performing the same task.","PeriodicalId":19076,"journal":{"name":"Nature neuroscience","volume":null,"pages":null},"PeriodicalIF":21.2,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41593-024-01704-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141790948","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}
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