报告人：Shinghua Ding, Associate professor
Dept. of Bioengineering, University of Missouri-Columbia, MO.
丁新华(Shinghua Ding)，现任美国密苏里大学生物工程系副教授，Dalton心血管研究中心研究员，长期从事神经生物学研究，在脑缺血神经传递作用及机制、星型胶质细胞、小胶质细胞、神经原相互作用研究上取得了卓越的成就，并在Journal of Neurochemistry, Glia, BMC Neuroscience, Journal of Cerebral Blood Flow & Metabolism 等国际知名刊物上发表学术论文20余篇。
Ca2+ signaling is a characteristic form of astrocyte excitability and has been suggested to mediate neurotransmitter release including glutamate from these cells. It has been known that G-protein coupled receptor (GPCR)-mediated Ca2+ elevation is the predominant Ca2+ signaling pathway in astrocytes. Pharmaceutical stimulations of GPCR in astrocytes induce synchronized Ca2+ oscillations among astrocytes, which are called Ca2+ wave. Similarly, electrical stimulation of neurons can also induce Ca2+ waves in astrocytes. However, during the last 20 years, those studies were done largely using cultured astrocytes. In this seminar I will present data of Ca2+ imaging in intact brain using two-photon microscopy. Our results showed that astrocytes in anaesthetized mice exhibit infrequent spontaneous Ca2+ increase; however, stimulations of different types of GPCR induce Ca2+ waves in astrocytes. I will further present data on astrocytic Ca2+ signaling and its role in neuronal toxicity in brain disorders including status epilepticus and ischemia.