Activity-dependent depression of GABAergic IPSCs in cultured hippocampal neurons

被引:54
作者
Jensen, K
Lambert, JDC
Jensen, MS
机构
[1] Univ Aarhus, Dept Physiol, DK-8000 Aarhus C, Denmark
[2] Univ Aarhus, Inst Anat, Dept Neurobiol, DK-8000 Aarhus, Denmark
关键词
D O I
10.1152/jn.1999.82.1.42
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Short term depression of monosynaptic GABAergic inhibitory postsynaptic currents (IPSCs) evoked between pairs of cultured rat hippocampal neurons was investigated using dual whole cell patch-clamp recordings. Paired stimuli applied to the GABAergic neuron resulted in paired-pulse depression (PPD) of the second IPSC (IPSC2) at interpulse intervals from 25 to 2,000 ms. CGP 55845A, but not CGP 35348, reduced PPD marginally. Brief paired-pulse applications of exogenous GABA indicated that postsynaptic factors made only minimal contribution to PPD of IPSCs. IPSC, and PPD was reduced on lowering [Ca2+](o) and enhanced on increasing [Ca2+](o). The potassium-channel blocker 4-aminopyridine (4-AP), which increases presynaptic Ca2+ influx, enhanced IPSCI and PPD. Chelation of residual Ca2+ in the GABAergic boutons with EGTA-AM enhanced PPD. Stimulation of the presynaptic neuron at frequencies (f) ranging from 2.5 to 80 Hz resulted in tetanic depression of IPSCs, which declined rapidly and reached a plateau depending on f and [Ca2+](o). CGP 55845A decreased tetanic depression in the first part of the train, but this could be overcome with continued stimulation. We show that GABAergic IPSCs are robustly depressed by paired-pulse stimulation in cultured hippocampal neurons. The depression of IPSCs is mainly independent of presynaptic GABA(B) receptors and could be caused by depletion of releasable vesicles. Depleted synapses recover with a slow time course, depending on factors that regulate [Ca2+](i) in the GABAergic boutons.
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页码:42 / 49
页数:8
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