PAIRED-PULSE DEPRESSION OF THE N-METHYL-D-ASPARTATE RECEPTOR-MEDIATED SYNAPTIC POTENTIALS IN THE AMYGDALA

被引:16
作者
HUANG, CC [1 ]
GEAN, PW [1 ]
机构
[1] NATL CHENG KUNG UNIV,COLL MED,DEPT PHARMACOL,TAINAN 70101,TAIWAN
关键词
N-METHYL-D-ASPARTATE RECEPTOR; GABA(B) RECEPTOR; PAIRED-PULSE DEPRESSION;
D O I
10.1111/j.1476-5381.1994.tb17096.x
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
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 gamma-aminobutyric acid(A) (GABA(A)) 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-guise 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 GABA(B) receptors. 5 Bath applications of Ba2+ or intracellular injection of Cs+ to block post- but not presynaptic GABA(B) 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 GABA(B) receptors to suppress the second e.p.s.p.(NMDA) via mechanisms other than activation of a postsynaptic GABA(B) receptor-coupled K+ conductance.
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页码:1029 / 1035
页数:7
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