{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T03:17:56Z","timestamp":1790911076528,"version":"4.1.0"},"reference-count":47,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2005,1,25]],"date-time":"2005-01-25T00:00:00Z","timestamp":1106611200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2005,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Brain\u2010derived neurotrophic factor (BDNF) regulates neuronal survival, neurite outgrowth, and excitatory synaptic transmission. We reported recently that acute BDNF exposure decreased \u03b3\u2010aminobutyric acid (GABA) responses in cultured mouse cerebellar granule cells through tyrosine receptor kinase B (TrkB) receptor\u2010mediated signaling. In the present study, we extend this work to investigate BDNF\u2010induced modulation of GABA responses and GABA<jats:sub>A<\/jats:sub> receptor\u2010mediated synaptic events in cerebellar slices. Thin (200 \u03bcm) parasagittal slices of cerebellum were prepared from postnatal Day 7 and 14 mice. Purkinje cells and granule cells, both of which express TrkB\u2010like immunoreactivity, were identified for whole\u2010cell recording. BDNF promptly enhanced GABA responses in Purkinje cells but, consistent with our previous finding in culture, attenuated those recorded in granule cells. In Purkinje cells, BDNF exposure shifted rightward the cumulative peak amplitude distribution for miniature inhibitory postsynaptic currents (mIPSCs) without changing the mIPSC frequency. BDNF\u2010induced potentiation of Purkinje cell responses to GABA was blocked by TrkB\u2010Fc (receptor body that sequesters BDNF), K252a (inhibitor of TrkB receptor autophosphorylation), U73122 (inhibitor of phospholipase\u2010C\u03b3 [PLC\u03b3]), KN62 (specific inhibitor of calcium\/calmodulin\u2010dependent kinase), KT5720 (specific cyclic AMP\u2010dependent kinase inhibitor), and by intracellular dialysis of Rp\u2010cyclic AMP or BAPTA (1,2\u2010bis(o\u2010aminophenoxy)ethane\u2010N,N, N\u2032,N\u2032\u2010tetraacetic acid). Overall, our results indicate that BDNF acutely potentiates GABA<jats:sub>A<\/jats:sub> receptor function in cerebellar Purkinje cells via the TrkB receptor\u2010PLC\u03b3 signal transduction cascade. In addition, we propose that cyclic AMP\u2010mediated intracellular signaling mechanisms may facilitate manifestation of the BDNF\u2010induced modulatory outcome. \u00a9 2005 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.20397","type":"journal-article","created":{"date-parts":[[2005,1,25]],"date-time":"2005-01-25T18:16:48Z","timestamp":1106677008000},"page":"616-627","source":"Crossref","is-referenced-by-count":36,"title":["PLC\u03b3 signaling underlies BDNF potentiation of Purkinje cell responses to GABA"],"prefix":"10.1002","volume":"79","author":[{"given":"Qing","family":"Cheng","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hermes 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