Type of Document	Thesis
Author	Zhong, Peng
Author's Email Address	pengzh@eng.fsu.edu
URN	etd-07132008-185640
Title	Na+ during DHPG Application Plays a Critical Role in DHPG-induced Inhibition of NMDA Receptor-mediated Synaptic Responses in CA1 Neurons.
Degree	Master of Science
Department	Chemical Engineering, Department of
Advisory Committee	Advisor Name Title Chi-Kai (Kevin) Chen Committee Chair Sachin Shanbhag Committee Member Xian-Min Yu Committee Member
Keywords	DHPG Synaptic Responses NMDA Receptor
Date of Defense	2008-06-30
Availability	unrestricted
Abstract Receptor trafficking such as endocytosis may decrease the number of surface receptors and hence down-regulate receptor-mediated functions. Previous studies showed that dynamic endocytosis of N-methyl-d-aspartate receptor/channels (NMDARs) inhibits the gating of remaining surface NMDARs characterized by a reduction in channel open duration. Surprisingly, the blockade of Na+ influx prevents the gating down-regulation of remaining surface NMDARs induced by NMDAR endocytosis. More importantly, if this gating down-regulation is prevented, NMDA channel endocytosis produces no change in NMDA channel-mediated whole-cell and synaptic responses. Here, I report that blocking Na+ influx only during (R,S)-3,5-dihydroxyphenylglycine (DHPG) application, which induces NMDA channel endocytosis, could effectively block the down-regulation of NMDA channel-mediated excitatory postsynaptic currents (EPSCs) induced by NMDA channel endocytosis in adult CA1 neurons. This finding provided the first evidence confirming that the Na+ influx blockade during DHPG application sufficiently prevents DHPG-induced down-regulation of NMDA channel-mediated synaptic responses in CA1 neurons.
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