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dc.contributor.authorYoshii, Akira
dc.contributor.authorConstantine-Paton, Martha
dc.date.accessioned2012-04-19T18:36:36Z
dc.date.available2012-04-19T18:36:36Z
dc.date.issued2010-02
dc.date.submitted2009-10
dc.identifier.issn1932-8451
dc.identifier.issn1932-846X
dc.identifier.urihttp://hdl.handle.net/1721.1/70067
dc.description.abstractBrain-derived neurotrophic factor (BDNF) is a prototypic neurotrophin that regulates diverse developmental events from the selection of neural progenitors to the terminal dendritic differentiation and connectivity of neurons. We focus here on activity-dependent synaptic regulation by BDNF and its receptor, full length TrkB. BDNF-TrkB signaling is involved in transcription, translation, and trafficking of proteins during various phases of synaptic development and has been implicated in several forms of synaptic plasticity. These functions are carried out by a combination of the three signaling cascades triggered when BDNF binds TrkB: The mitogen-activated protein kinase (MAPK), the phospholipase Cγ (PLC PLCγ), and the phosphatidylinositol 3-kinase (PI3K) pathways. MAPK and PI3K play crucial roles in both translation and/or trafficking of proteins induced by synaptic activity, whereas PLCγ regulates intracellular Ca2+ that can drive transcription via cyclic AMP and a protein kinase C. Conversely, the abnormal regulation of BDNF is implicated in various developmental and neurodegenerative diseases that perturb neural development and function. We will discuss the current state of understanding BDNF signaling in the context of synaptic development and plasticity with a focus on the postsynaptic cell and close with the evidence that basic mechanisms of BDNF function still need to be understood to effectively treat genetic disruptions of these pathways that cause devastating neurodevelopmental diseases.en_US
dc.description.sponsorshipUnited States. Dept. of Defense (contract grant number: TS080074)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Contract grant number: R01EY014074)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Contract grant number: R01EY006039)en_US
dc.language.isoen_US
dc.publisherWiley-Blackwell Pubishersen_US
dc.relation.isversionofhttp://dx.doi.org/10.1002/dneu.20765en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alike 3.0en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/en_US
dc.sourcePubMed Centralen_US
dc.titlePostsynaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity, and Diseaseen_US
dc.typeArticleen_US
dc.identifier.citationYoshii, Akira, and Martha Constantine-Paton. “Postsynaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity, and Disease.” Developmental Neurobiology (2010): 304–322.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Brain and Cognitive Sciencesen_US
dc.contributor.departmentMcGovern Institute for Brain Research at MITen_US
dc.contributor.approverConstantine-Paton, Martha
dc.contributor.mitauthorConstantine-Paton, Martha
dc.contributor.mitauthorYoshii, Akira
dc.relation.journalDevelopmental Neurobiologyen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsYoshii, Akira; Constantine-Paton, Marthaen
dc.identifier.orcidhttps://orcid.org/0000-0003-2268-0863
mit.licenseOPEN_ACCESS_POLICYen_US
mit.metadata.statusComplete


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