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谷氨酸性突触在痛觉和记忆中的突触和分子机制
作者姓名:Zhuo  M
作者单位:华盛顿大学医学院麻醉系、解剖及神经生物学系、精神病学系,华盛顿大学痛觉中心,美国圣路易州,63110
基金项目:ThisworkwassupportedinpartbygrantsfromtheNINDS (NS38680 )andNIDA (DA10 833)
摘    要:谷氨酸是哺乳动物脑中的兴奋性递质。中枢神经系统的谷氨酸性突触广泛参与痛觉传递,突触可塑性和递质的调节。谷氨酸的NMDA受体参与前脑相关的学习及功能。在这篇综述中,我们提出前脑的NMDA受体通过增强谷氨酸性突触传递导致长期性的炎痛。具有增强NMDA受体功能的小鼠会产生更多的慢性痛。NMDA NR2B受体抑制剂在未来可能被用来控制人类的慢性痛。

关 键 词:谷氨酸  突触  痛觉  记忆  小鼠

Synaptic and molecular mechanisms of glutamatergic synapses in pain and memory
Zhuo M.Synaptic and molecular mechanisms of glutamatergic synapses in pain and memory[J].Acta Physiologica Sinica,2003,55(1):1-8.
Authors:Zhuo Min
Institution:Washington University Pain Center, Departments of Anesthesiology, Anatomy Neurobiology and Psychiatry, Washington University School of Medicine, St. Louis, MO 63110, USA. E-mail: Zhuom@morpheus.wustl.edu
Abstract:Glutamate is a fast excitatory transmitter in mammalian brains. Glutamatergic synapses are found in central regions related to pain transmission, plasticity and modulation. Glutamate NMDA receptors in forebrain structures are well known to contribute to the formation and storage of information. Here we propose the hypothesis that forebrain NMDA receptors play an important role in persistent inflammatory pain by re enforcing glutamate sensory transmission in the brain. Mice with enhanced function of forebrain NMDA receptors demonstrate selective enhancement of persistent pain and allodynia. Drugs targeting forebrain NMDA NR2B receptors may serve as a new class of medicine to control persistent pain in humans.
Keywords:glutamate  synapse  pain memory  mice
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