卓敏教授系列学术报告之一(医学部)

发布者:系统管理员发布时间:2008-04-24浏览次数:142


Genetic and Molecular Studies of Mind: Memory, Emotion and Mental Diseases

报告人:卓敏 教授

EJLB-Smith Chair, Canada Research Chair, Professor, University of Toronto

卓敏教授简介:

Dr. Zhuo is a Professor of Physiology, University of Toronto. He is the Michael Smith Chair in Neuroscience and Mental Health, and the Canada Research Chair in Pain and Cognition. He received his Ph.D. in the University of Iowa, and postdoctoral trainings at Columbia University and Stanford University. He held a faculty position at Washington University in St. Louis, before he moved to University of Toronto. He is also the editor-in-chief for the first online journal of Molecular Pain. He is Chang Jiang Scholar in Fudan University, Shanghai, China.

在国际权威杂志如NatureScienceNeuronNature NeurosciJ Neurosci等杂志上发表研究论文100余篇、综述10余篇。

拥有6项有关新药研制的美国专利。

主要研究方向:

中枢学习记忆机制

痛觉传递的中枢可塑性及其突触分子机制

焦虑和其他精神病机制

报告摘要:

Recent studies suggest that the brain continually and dynamically reorganizes itself. Synapses, the physical connections between neurons in the brain, can undergo long-term plastic changes throughout life. Studies of molecular and cellular mechanisms of such changes not only provide important insight into how we learn and store new knowledge in our brains, but also reveal the molecular mechanisms of pathological changes, as well as new drug target for the treatment of brain diseases.

Pain is the unpleasant experience or sensation induced by noxious stimuli. Painful information enters the brain through spinal-brain projecting systems, and projecting to widely different brain areas. Most of all, painful inputs enter the forebrain areas including the Anterior cingulate cortex ACC, and trigger unpleasant sensation or experience. Painful inputs projected into the somatosensory cortex help to determine the location and quality of painful stimuli. Hippocampus, a structure known to be important for spatial memory, is also activated by painful stimuli, and may contribute to the formation of pain-related spatial memory. Neuronal inputs into the amygdala are critical for forming fear memory and pain-modulation. Here I propose here that plastic changes in synaptic responses as well as structures may contribute to fear memory and painful sufferings.

I propose that increasing the synaptic strength in the ACC help to store fearful information in the brain. Using different and new experimental methods, we have identified several key molecules in helping enhance synaptic strength in the ACC. Upon a painful electric shock, excitatory neurotransmitter glutamate is released in the brain synapse such as those in the ACC. Activation of various glutamate receptors in synapses can lead to increases in intracellular calcium levels. We found that one major member of glutamate receptors called NMDA receptor is critical for causing postsynaptic calcium increases. Activation of NMDA receptors, including the NR2A and NR2B subunits, are required for the induction of ACC LTP. The enhancement of postsynaptic AMPA receptor mediated responses is critical for the expression of ACC LTP. Following peripheral painful stimulus, synaptic transmission in the ACC undergoes both pre- and post-synaptic changes. In freely moving animals, focal electrical stimulation of the ACC generates emotional ultrasonic vocalization, and forms emotional fear memory, that last at least for several days. Genetic or pharmacological inhibition of local NMDA NR2B receptors in the ACC reduces LTP and impairs behavioral fear memory.

Clinical implications

Fear and pain are likely results of long-term plastic changes in the ACC and related areas. Drugs developed based on ACC plasticity may selectively treat chronic fear, anxiety and pain in patients with cancer, AIDS, and other mental diseases.

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