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Enhancement of augmentation in the entorhinal excitatory responses during the progress of Amygdala kindling.

杏仁核点燃过程中内嗅兴奋反应的增强。

基本信息

批准号：
06680790
负责人：
MATSUURA Shiushi
金额：
$ 1.34万
依托单位：
Osaka City University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

项目摘要

Entorhinal posttetanic responses (PTRs) to 10 single (0.3Hz) stimuli immediately after train stimulus (10Hz, 100 pulses) to the amygdala were recorded from conscious rats, which had electrodes previously implanted under pentobarbital anesthesia, and the magnitude of PTRs was estimated as the area between the negative potential ascribable to excitatory activation in the averaged PTR and the baseline. When the stimulus intensity was 50-100 mA lower than threshold to induce afterdischarges (ADs), the averaged PTR showed the same magnitude as the averaged test response before train, showing no augmentation in the PTR.However, augmentation in the PTR was apparent at the intensity 25 mA lower than the AD threshold and progressively increased untill the intensity became the AD threshold. The magnitude of the averaged PTR (except for some 1-3 PTRs superimposed on ADs) was more markedly increased and showed a linear relation to the AD duration, when train stimulus with the AD threshold intensity was repeated untill the AD duration became about 30 s. The increase of PTR first occurred in the mono- and later in the polysynaptic component during the developmental stages of kindling. In the hippocampal PTRs, augmentation became to be increased more latoly than in the entorhinal cortex. An NMDA receptor antagonist (CPP) and GABA receptor agonist (pentobarbital) markedly deppressed ADs and blocked kindling seizures in association with a decrease in augmentation in PTRs. These results indicate that enhancement of augmentation based on NMDA receptor activation in the PTR is involved in the origin of development of ADs and seizures during the early course of kindling.

在戊巴比妥钠麻醉下，预先植入电极的清醒大鼠，在连续刺激（10 Hz，100个脉冲）杏仁核后立即记录10个单次（0.3Hz）刺激的内嗅强直后反应（PTRs），PTRs的大小估计为平均PTR中归因于兴奋性激活的负电位与基线之间的面积。当刺激强度低于阈值50-100 mA时，平均PTR与训练前的平均测试反应相同，没有增加，但当刺激强度低于阈值25 mA时，PTR明显增加，并逐渐增加，直至达到阈值。当重复AD阈值强度的训练刺激直至AD持续时间达到约30 s时，平均PTR（除了叠加在AD上的一些1-3个PTR）的幅度更加明显增加，并与AD持续时间呈线性关系。在点燃的发育阶段，PTR的增加首先发生在单突触成分，然后在多突触成分。在海马PTRs中，增强变得比内嗅皮层中的增强更多。NMDA受体拮抗剂（CPP）和GABA受体激动剂（戊巴比妥）显着depressed AD和阻断点燃癫痫发作与减少增加PTRs。这些结果表明，增强增强的基础上NMDA受体激活的PTR参与的起源发展的AD和癫痫发作在点燃的早期过程。