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

• Other Authors: Zhong, Peng (authoraut)
• Format: Others
• Language: English; English
• Published: Florida State University
• Subjects: Chemical engineering
• Online Access: http://purl.flvc.org/fsu/fd/FSU_migr_etd-0522

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.