We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Postsynaptic TRPC1 Function Contributes to BDNF-Induced Synaptic Potentiation at the Developing Neuromuscular Junction.
- Authors
McGurk, Julie S.; Shim, Sangwoo; Kim, Ju Young; Wen, Zhexing; Song, Hongjun; Ming, Guo-li
- Abstract
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.
- Subjects
NEUROTROPHINS; NEURAL transmission; TRP channels; CELL junctions; SYNAPSES; CENTRAL nervous system; NEUROPLASTICITY; XENOPUS
- Publication
Journal of Neuroscience, 2011, Vol 31, Issue 41, p14754
- ISSN
0270-6474
- Publication type
Article
- DOI
10.1523/JNEUROSCI.3599-11.2011