海马体CA1神经元中突触前和突触后活动的配对诱导了NMDA受体介导的突触电位的长期改变。

Pairing of pre- and postsynaptic activities in hippocampal CA1 neurons induces long-term modifications of NMDA receptor-mediated synaptic potential.

作者信息

Lin J H, Way L J, Gean P W

机构信息

Department of Pharmacology, College of Medicine, National Cheng-Kung University, Tainan, Taiwan.

出版信息

Brain Res. 1993 Feb 12;603(1):117-20. doi: 10.1016/0006-8993(93)91306-d.

DOI:10.1016/0006-8993(93)91306-d

PMID:8095836

Abstract

An in vitro slice preparation of rat hippocampus was used to study the long-term modifications of pharmacologically isolated N-methyl-D-aspartate (NMDA) receptor-mediated excitatory postsynaptic potential (EPSPNMDA). Intracellular recordings were made from CA1 pyramidal cells in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) and picrotoxin (50 microM) which block non-NMDA and GABAA receptors, respectively. Pairing of low-frequency EPSPNMDA with postsynaptic depolarization induced a long-term depression (LTD) of EPSPNMDA. The maximal reduction of EPSPNMDA amplitude amounted to 81.3% of the control 1 min after the pairing. When low-frequency synaptic stimulation was paired with strong postsynaptic depolarization, a long-term potentiation (LTP) of EPSPNMDA could be induced. These results suggest that the induction of long-term modifications of EPSPNMDA has at least a postsynaptic component.

摘要

采用大鼠海马体的体外脑片制备技术，研究药理学分离的N-甲基-D-天冬氨酸（NMDA）受体介导的兴奋性突触后电位（EPSPNMDA）的长期变化。在分别阻断非NMDA和GABAA受体的6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX；10微摩尔）和苦味毒素（50微摩尔）存在的情况下，对CA1锥体神经元进行细胞内记录。低频EPSPNMDA与突触后去极化配对可诱导EPSPNMDA的长期抑制（LTD）。配对后1分钟，EPSPNMDA幅度的最大降低量达到对照的81.3%。当低频突触刺激与强突触后去极化配对时，可诱导EPSPNMDA的长期增强（LTP）。这些结果表明，EPSPNMDA长期变化的诱导至少有一个突触后成分。