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Na+ during Dhpg Application Plays a Critical Role in DHPG-Induced Inhibition of NMDA Channel-Mediated Synaptic Responses in CA1 Neurons

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. / A Thesis submitted to the Department of Chemical & Biomedical Engineering in
partial fulfillment of the requirements for the degree of Master of Science. / Degree Awarded: Summer Semester, 2008. / Date of Defense: June 30, 2008. / DHPG, Synaptic Responses, NMDA Receptor / Includes bibliographical references. / Chi-Kai (Kevin) Chen, Professor Directing Thesis; Xian-Min Yu, Committee Member; Sachin Shanbhag, Committee Member.

Identiferoai:union.ndltd.org:fsu.edu/oai:fsu.digital.flvc.org:fsu_168678
ContributorsZhong, Peng (authoraut), Chen, Chi-Kai (Kevin) (professor directing thesis), Yu, Xian-Min (committee member), Shanbhag, Sachin (committee member), Department of Chemical and Biomedical Engineering (degree granting department), Florida State University (degree granting institution)
PublisherFlorida State University
Source SetsFlorida State University
LanguageEnglish, English
Detected LanguageEnglish
TypeText, text
Format1 online resource, computer, application/pdf

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