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大鼠纹状体神经元中兴奋性突触输入的抑制

Depression of excitatory synaptic input in rat striatal neurons.

作者信息

Walsh J P

机构信息

Ethel Percy Andrus Gerontology Center, USC Program in Neurosciences, University of Southern California, Los Angeles 90089-0191.

出版信息

Brain Res. 1993 Apr 9;608(1):123-8. doi: 10.1016/0006-8993(93)90782-i.

DOI:10.1016/0006-8993(93)90782-i
PMID:8495336
Abstract

Intracellular recording of rat striatal neurons was performed in vitro to investigate posttetanic changes in the excitatory post-synaptic potential (EPSP) elicited by stimulation of the corpus callosum. Tetanic stimulation induced posttetanic potentiation (PTP) in 11 of 12 cells. The PTP decayed in 1-5 min and was followed by either a short or long duration depression of the EPSP in 10 of 12 neurons. The remaining two neurons examined showed a slight enhancement of the EPSP that lasted for 30 min after the tetanus. The group of cells demonstrating short-duration depression (n = 3) were characterized by a decay of the depression to the control level by 15-20 min post-tetanus. The EPSP in the remaining cells showing depression (n = 7) showed a maintained depression for the entire recording session. Blockade of GABAA receptors with bicuculline (30 microM) or NMDA receptors with APV (50 microM) did not effect the induction of long-lasting depression of the striatal EPSP. The data indicates that the corticostriatal pathway can undergo enduring forms of use-dependent synaptic plasticity. This type of synaptic modification may participate in the refinement of movement and contribute to striatal related learning and memory.

摘要

在体外对大鼠纹状体神经元进行细胞内记录,以研究刺激胼胝体引起的兴奋性突触后电位(EPSP)的强直后变化。强直刺激在12个细胞中的11个中诱导了强直后增强(PTP)。PTP在1 - 5分钟内衰减,随后12个神经元中的10个出现EPSP的短期或长期抑制。其余两个被检查的神经元在破伤风后显示EPSP轻微增强,持续30分钟。表现出短期抑制的细胞组(n = 3)的特征是,在破伤风后15 - 20分钟,抑制衰减至对照水平。其余表现出抑制的细胞(n = 7)的EPSP在整个记录过程中保持抑制。用荷包牡丹碱(30微摩尔)阻断GABAA受体或用APV(50微摩尔)阻断NMDA受体并不影响纹状体EPSP的持久抑制的诱导。数据表明,皮质纹状体通路可以经历持久形式的使用依赖性突触可塑性。这种类型的突触修饰可能参与运动的精细化,并有助于与纹状体相关的学习和记忆。

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