{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,28]],"date-time":"2025-09-28T20:31:42Z","timestamp":1759091502614},"reference-count":55,"publisher":"Society for Neuroscience","issue":"41","license":[{"start":{"date-parts":[[2012,4,12]],"date-time":"2012-04-12T00:00:00Z","timestamp":1334188800000},"content-version":"vor","delay-in-days":183,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-sa\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Neurosci."],"published-print":{"date-parts":[[2011,10,12]]},"abstract":"<jats:p>Brain-derived neurotrophic factor (BDNF) induces synaptic potentiation at both neuromuscular junctions (NMJs) and synapses of the CNS through a Ca<jats:sup>2+<\/jats:sup>-dependent pathway. The molecular mechanism underlying BDNF-induced synaptic potentiation, especially the regulation of Ca<jats:sup>2+<\/jats:sup>dynamics, is not well understood. Using the<jats:italic>Xenopus<\/jats:italic>NMJ in culture as a model system, we show that pharmacological inhibition or morpholino-mediated knockdown of<jats:italic>Xenopus<\/jats:italic>TRPC1 (XTRPC1) significantly attenuated the BDNF-induced potentiation of the frequency of spontaneous synaptic responses at the NMJ. Functionally, XTRPC1 was required specifically in postsynaptic myocytes for BDNF-induced Ca<jats:sup>2+<\/jats:sup>elevation and full synaptic potentiation at the NMJ, suggesting a previously underappreciated postsynaptic function of Ca<jats:sup>2+<\/jats:sup>signaling in neurotrophin-induced synaptic plasticity, in addition to its well established role at presynaptic sites. Mechanistically, blockade of the p75 neurotrophin receptor abolished BDNF-induced postsynaptic Ca<jats:sup>2+<\/jats:sup>elevation and restricted BDNF-induced synaptic potentiation, while knockdown of the TrkB receptor in postsynaptic myocytes had no effect. Our study suggests that BDNF-induced synaptic potentiation involves coordinated presynaptic and postsynaptic responses and identifies TRPC1 as a molecular mediator for postsynaptic Ca<jats:sup>2+<\/jats:sup>elevation required for BDNF-induced synaptic plasticity.<\/jats:p>","DOI":"10.1523\/jneurosci.3599-11.2011","type":"journal-article","created":{"date-parts":[[2011,10,12]],"date-time":"2011-10-12T17:02:13Z","timestamp":1318438933000},"page":"14754-14762","source":"Crossref","is-referenced-by-count":18,"title":["Postsynaptic TRPC1 Function Contributes to BDNF-Induced Synaptic Potentiation at the Developing Neuromuscular Junction"],"prefix":"10.1523","volume":"31","author":[{"given":"Julie S.","family":"McGurk","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sangwoo","family":"Shim","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ju 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