Paired‐pulse depression of the N‐methyl‐D‐aspartate receptor‐mediated synaptic potentials in the amygdala
Paired‐pulse depression of the N‐methyl‐D‐aspartate receptor‐mediated synaptic potentials in the amygdala
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N-甲基-D-天冬氨酸受体介导的杏仁核突触电位的配对脉冲抑制
DOI：
10.1111/j.1476-5381.1994.tb17096.x
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发表时间：
1994
影响因子：
7.3
通讯作者：
P. Gean
中科院分区：
文献类型：
--
作者：
Chiung‐Chun Huang;P. Gean
1采用体外大鼠杏仁核切片制备方法，研究配对脉冲抑制N -甲基- D -天冬氨酸（NMDA）受体介导的突触电位e.p.s.p.NMDA。2采用含有非NMDA受体拮抗剂、6‐氰基‐7‐硝基喹啉‐2,3‐二酮（CNQX）和γ‐氨基丁酸（GABAA）阻滞剂微毒素的溶液，增加刺激强度，从药理学上分离e.p.s.p.NMDA。当连续施加两种相同强度的刺激时，第二个e.p.s.p.NMDA被抑制。这种配对脉冲抑制在刺激间隔为100 ms至2000 ms时出现；在间隔200 ms时观察到最大的抑制。4过量的苯氯芬或2 -羟基苯氯芬抑制了配对脉冲抑制，表明GABAB受体参与其中。Ba2+或细胞内注射Cs+阻断突触后而非突触前GABAB受体未能抑制配对脉冲抑制（PPD）。百日咳毒素对巴氯芬诱导的突触后超极化有抑制作用。然而，e.p.s.p.NMDA的PPD不受百日咳毒素处理的影响。这些结果表明，第一刺激释放的GABA通过激活突触后GABAB受体偶联的K+电导以外的机制作用于GABAB受体抑制第二e.p.s.p.NMDA。
1 An in vitro slice preparation of rat amygdala was used to study the paired‐pulse depression of the N‐methyl‐D‐aspartate (NMDA) receptor‐mediated synaptic potential e.p.s.p.NMDA. 2 The e.p.s.p.NMDA was isolated pharmacologically by applying a solution containing the non‐NMDA receptor antagonist, 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX) and the γ‐aminobutyric acidA (GABAA) blocker picrotoxin and increasing the stimulus intensity. 3 When two stimuli of identical strength were applied in close succession, the second e.p.s.p.NMDA was depressed. This paired‐pulse depression was seen with interstimulus intervals of between 100 ms and 2000 ms; the maximal depression was observed at interval of 200 ms. 4 Superfusion of phaclofen or 2‐hydroxy‐saclofen inhibited the paired‐pulse depression indicating the involvement of GABAB receptors. 5 Bath applications of Ba2+ or intracellular injection of Cs+ to block post‐ but not presynaptic GABAB receptors failed to inhibit the paired‐pulse depression (PPD). 6 Incubation of slices with pertussis toxin prevented the postsynaptic hyperpolarization induced by baclofen. The PPD of e.p.s.p.NMDA, however, was not affected by pertussis toxin treatment. 7 These results suggest that GABA released by the first stimulus acts on GABAB receptors to suppress the second e.p.s.p.NMDA via mechanisms other than activation of a postsynaptic GABAB receptor‐coupled K+ conductance.
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影响因子：
2.5
作者：
D. Rainnie;E. Asprodini;P. Shinnick‐Gallagher
通讯作者：
D. Rainnie;E. Asprodini;P. Shinnick‐Gallagher
巴氯芬对大鼠齿状回具有促癫痫作用。
DOI：
--
发表时间：
1989
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Mott,DD;Bragdon,AC;Lewis,DV;Wilson,WA
通讯作者：
Wilson,WA
影响因子：
2.5
作者：
D. Rainnie;E. Asprodini;P. Shinnick‐Gallagher
通讯作者：
D. Rainnie;E. Asprodini;P. Shinnick‐Gallagher
点燃引起基底外侧杏仁核突触传递的持久变化。
影响因子：
2.5
作者：
Rainnie,DG;Asprodini,EK;Shinnick-Gallagher,P
通讯作者：
Shinnick-Gallagher,P
巴氯芬在低浓度下抑制海马癫痫样活动，而不抑制突触传递。
DOI：
--
发表时间：
1986
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Swartzwelder,HS;Bragdon,AC;Sutch,CP;Ault,B;Wilson,WA
通讯作者：
Wilson,WA