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dc.contributor.authorFaust, Travis E.
dc.contributor.authorGunner, Georgia
dc.contributor.authorSchafer, Dorothy P
dc.date2022-08-11T08:08:28.000
dc.date.accessioned2022-08-23T15:56:25Z
dc.date.available2022-08-23T15:56:25Z
dc.date.issued2021-11-01
dc.date.submitted2022-01-31
dc.identifier.citation<p>Faust TE, Gunner G, Schafer DP. Mechanisms governing activity-dependent synaptic pruning in the developing mammalian CNS. Nat Rev Neurosci. 2021 Nov;22(11):657-673. doi: 10.1038/s41583-021-00507-y. Epub 2021 Sep 20. PMID: 34545240; PMCID: PMC8541743. <a href="https://doi.org/10.1038/s41583-021-00507-y">Link to article on publisher's site</a></p>
dc.identifier.issn1471-003X (Linking)
dc.identifier.doi10.1038/s41583-021-00507-y
dc.identifier.pmid34545240
dc.identifier.urihttp://hdl.handle.net/20.500.14038/29964
dc.description.abstractAlmost 60 years have passed since the initial discovery by Hubel and Wiesel that changes in neuronal activity can elicit developmental rewiring of the central nervous system (CNS). Over this period, we have gained a more comprehensive picture of how both spontaneous neural activity and sensory experience-induced changes in neuronal activity guide CNS circuit development. Here we review activity-dependent synaptic pruning in the mammalian CNS, which we define as the removal of a subset of synapses, while others are maintained, in response to changes in neural activity in the developing nervous system. We discuss the mounting evidence that immune and cell-death molecules are important mechanistic links by which changes in neural activity guide the pruning of specific synapses, emphasizing the role of glial cells in this process. Finally, we discuss how these developmental pruning programmes may go awry in neurodevelopmental disorders of the human CNS, focusing on autism spectrum disorder and schizophrenia. Together, our aim is to give an overview of how the field of activity-dependent pruning research has evolved, led to exciting new questions and guided the identification of new, therapeutically relevant mechanisms that result in aberrant circuit development in neurodevelopmental disorders.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=34545240&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1038/s41583-021-00507-y
dc.subjectCellular neuroscience
dc.subjectSynaptic development
dc.subjectDevelopmental Neuroscience
dc.subjectMolecular and Cellular Neuroscience
dc.titleMechanisms governing activity-dependent synaptic pruning in the developing mammalian CNS
dc.typeJournal Article
dc.source.journaltitleNature reviews. Neuroscience
dc.source.volume22
dc.source.issue11
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3199&amp;context=faculty_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/2166
dc.identifier.contextkey27891363
refterms.dateFOA2022-08-23T15:56:25Z
html.description.abstract<p>Almost 60 years have passed since the initial discovery by Hubel and Wiesel that changes in neuronal activity can elicit developmental rewiring of the central nervous system (CNS). Over this period, we have gained a more comprehensive picture of how both spontaneous neural activity and sensory experience-induced changes in neuronal activity guide CNS circuit development. Here we review activity-dependent synaptic pruning in the mammalian CNS, which we define as the removal of a subset of synapses, while others are maintained, in response to changes in neural activity in the developing nervous system. We discuss the mounting evidence that immune and cell-death molecules are important mechanistic links by which changes in neural activity guide the pruning of specific synapses, emphasizing the role of glial cells in this process. Finally, we discuss how these developmental pruning programmes may go awry in neurodevelopmental disorders of the human CNS, focusing on autism spectrum disorder and schizophrenia. Together, our aim is to give an overview of how the field of activity-dependent pruning research has evolved, led to exciting new questions and guided the identification of new, therapeutically relevant mechanisms that result in aberrant circuit development in neurodevelopmental disorders.</p>
dc.identifier.submissionpathfaculty_pubs/2166
dc.contributor.departmentSchafer Lab
dc.contributor.departmentNeurobiology
dc.contributor.departmentGraduate School of Biomedical Sciences, Neuroscience Program
dc.source.pages657-673
dc.contributor.studentGeorgia Gunner
dc.description.thesisprogramNeuroscience


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