CALCIUM-CHANNEL INVOLVEMENT IN GABA(B) RECEPTOR-MEDIATED INHIBITION OF GABA RELEASE IN AREA CA1 OF THE RAT HIPPOCAMPUS
CALCIUM-CHANNEL INVOLVEMENT IN GABA(B) RECEPTOR-MEDIATED INHIBITION OF GABA RELEASE IN AREA CA1 OF THE RAT HIPPOCAMPUS
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DOI：
10.1152/jn.1995.74.1.43
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发表时间：
1995-07-01
影响因子：
2.5
通讯作者：
MADISON, DV
中科院分区：
文献类型：
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作者：
DOZE, VA;COHEN, GA;MADISON, DV
1.在大鼠海马脑片中进行实验以检查抑制性突触传递的GABA能抑制的性质。在这些实验中，使用诱发抑制性突触后电位（IPSP）的细胞内记录和自发GABA能抑制性突触后电流（IPSC）的全细胞记录来测试γ-氨基丁酸-B（GABA（B））受体激动剂巴氯芬和亚型选择性钙通道阻滞剂的作用。2.巴氯芬抑制GABA（A）介导的诱发性和自发性（动作电位依赖性）单突触IPSP和IPSC，但对CA 1锥体神经元中记录的河豚毒素抗性（动作电位非依赖性）微型IPSC的频率没有影响.通过提高细胞外钾离子浓度使GABA能突触末梢去极化，引起动作电位独立的微型IPSC频率增加，这可以被巴氯芬或镉（电压依赖性钙通道的阻滞剂）抑制。此外，在这些去极化条件下，镉封闭了巴氯芬对微型IPSCs的抑制作用。这些数据表明，巴氯芬只减少去极化诱导的，而不是量子，GABA的释放，它这样做是通过减少突触前电压依赖性钙流入。亚型选择性钙通道阻滞剂的实验表明，巴氯芬的突触前作用是通过ω-芋螺毒素-GVIA敏感性和ω-龙舌兰毒素-IVA敏感性介导的，但不是二氢吡啶敏感性钙通道。
1. Experiments were performed in rat hippocampal slices to examine the nature of GABAergic inhibition of inhibitory synaptic transmission. In these experiments the effects of the gamma-aminobutyric acid-B (GABA(B)) receptor agonist, baclofen, and of subtype-selective calcium channel blockers were tested with the use of intracellular recordings of evoked inhibitory postsynaptic potentials (IPSPs) and whole cell recordings of spontaneous GABAergic inhibitory postsynaptic currents (IPSCs).2. Baclofen inhibited evoked and spontaneous (action-potential- dependent) monosynaptic GABA(A)-mediated IPSPs and IPSCs but had no effect on the frequency of tetrodotoxin-resistant (action-potential-independent) miniature IPSCs recorded in CA1 pyramidal neurons.3. Depolarizing GABAergic synaptic terminals by raising the extracellular potassium concentration caused an increase in action-potential-independent miniature IPSC frequency that could be inhibited by either baclofen or cadmium, a blocker of voltage-dependent calcium channels. In addition, under these depolarizing conditions, cadmium occluded the baclofen inhibition of miniature IPSCs. These data suggest that baclofen reduces only depolarization-induced, not quantal, GABA release and that it does so by decreasing presynaptic voltage-dependent calcium influx.4. Experiments with subtype-selective calcium channel blockers demonstrate that the presynaptic action of baclofen was mediated through both omega-conotoxin-GVIA-sensitive and omega-agatoxin-IVA-sensitive, but not dihydropyridine-sensitive calcium channels.