报告题目: Metabotropic neurotransmission: message taken and reported through G protein-regulated ion channels
报告人: Dr. Michael Xi Zhu, professor of University of Texas Health Science Center at Houston
主持人: 李晓涛 教授
报告时间: 11月23日 10:00 （周三上午）
报告地点: 天美娱乐534报告厅
报告人简介：Michael Xi Zhu is professor of Department of Integrative Biology and Pharmacology, McGovern Medical School, the University of Texas Health Science Center at Houston, Houston, Texas. He received his B.S. degree in Biology from Fudan University, Shanghai, China, in 1984, and his M.S. and Ph.D. degrees from University of Houston, Houston, Texas, USA, in 1988 and 1991, respectively. He had his postdoctoral training in Cellular and Molecular Biology from 1991-1994 at Baylor College of Medicine. He then worked as an Assistant Researcher in the Department of Anesthesiology, UCLA, from 1994 to 1997. In autumn of 1997, he went to the Ohio State University to build his own lab and rose from the rank of Assistant Professor to Full Professor in the Department of Neuroscience there. In 2010, he moved to his current position at the University of Texas-Houston. Dr. Zhu’s research interests include several aspects of cell signaling, especially those that involve heterotrimeric G proteins and ion channels that affect Ca2+ signaling. He has published more than 130 research papers, reviews, and monographs on these topics and delivered lectures at many international conferences and symposia. Dr. Zhu’s main contributions include identification and characterization of multiple Transient Receptor Potential Canonical (TRPC) channels in mammalian species and determination of the molecular identity of endolysosomal Ca2+ release channels activated by the Ca2+ mobilizing messenger, nicotinic acid adenine dinucleotide phosphate (NAADP). Dr. Zhu is a regular member of the Biophysical Society, Aspet and ASMBM. He is Series Editors of the CRC Methods in Signal Transduction Book Series, an Associate Editor of Journal of Cellular Physiology and a member of editorial boards of Pflügers Archiv European Journal of Physiology, Biophysics Reports and Molecular Pharmacology.
报告内容🧾：In a neural network, neurons frequently receive multiple coincidental transmitter inputs representing varying activities of different brain regions. These inputs not only vary in the signal pathways they activate but also in the strengths for each of the pathways. However, it remains unclear how neurons decipher co-incident inputs of varying strengths and encode discernible output messages. The vast majority of neurotransmitters signal through G protein-coupled receptors, which activate heterotrimeric G proteins to alter neuronal function via a limited set of effectors, including G protein-activated and/or receptor-operated channels that are capable of modulating neuronal excitability. For receptors that couple to Gq/11 and Gi/o, whereas the activation of Gq/11-phospholipase C pathway, which hydrolyzes phosphatidylinositol 4,5-bisphosphate, suppresses Gi/o-mediated activation of G protein-activated inwardly rectifying K+ (GIRK) channels, the phospholipase C signaling is required for Gi/ostimulation of the nonselective cation channel, Transient Receptor Potential Canonical 4 (TRPC4). Thus, coincident activation of Gq/11 and Gi/opathways differentially affects GIRK and TRPC4 channel activities, shaping excitability in a manner that is very sensitive on the relative strengths of Gq/11 and Gi/o signaling. Using whole-cell slice recordings and agonist or electrical stimulation of lateral septal neurons, we demonstrate that varying stimulation intensities at Gq/11 and Gi/o-coupled receptors give rise to distinctive membrane potential waveforms that include burst firing, plateau depolarization and hyperpolarization of varying durations resulting from combined actions of TRPC4 and GIRK channels. These differential responses alter neuronal firing in distinguishable patterns. We propose that the conversion of concurrent Gq/11 and Gi/o signaling of differential strengths into discernible electrical responses by joint actions of TRPC4 and GIRK channels is vital for lateral septum to serve as the information processing center of cerebrum for higher-order brain functions.
