التفاصيل البيبلوغرافية
| العنوان: |
Postsynaptic TRPC1 Function Contributes to BDNF-Induced Synaptic Potentiation at the Developing Neuromuscular Junction. |
| المؤلفون: |
McGurk, Julie S., Shim, Sangwoo, Kim, Ju Young, Wen, Zhexing, Song, Hongjun, Ming, Guo-li |
| المصدر: |
Journal of Neuroscience; 10/12/2011, Vol. 31 Issue 41, p14754-14762, 9p |
| مصطلحات موضوعية: |
NEUROTROPHINS, NEURAL transmission, TRP channels, CELL junctions, SYNAPSES, CENTRAL nervous system, NEUROPLASTICITY, XENOPUS |
| مستخلص: |
Brain-derived neurotrophic factor (BDNF) induces synaptic potentiation at both neuromuscular junctions (NMJs) and synapses of the CNS through a Ca2β-dependent pathway. The molecular mechanism underlying BDNF-induced synaptic potentiation, especially the regulation of Ca2βdynamics, is not well understood. Using the XenopusNMJin culture as a model system, we show that pharmacological inhibition or morpholino-mediated knockdown of Xenopus 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 Ca2β elevation and full synaptic potentiation at the NMJ, suggesting a previously underappreciated postsynaptic function of Ca2β 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 Ca2βelevation and restricted BDNFinduced 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 Ca2β elevation required for BDNF-induced synaptic plasticity. [ABSTRACT FROM AUTHOR] |
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