Pfrieger F W, Gottmann K, Lux H D
Max-Planck-Institute for Psychiatry, Department of Neurophysiology, Planegg-Martinsried, Germany.
Neuron. 1994 Jan;12(1):97-107. doi: 10.1016/0896-6273(94)90155-4.
The time courses of the gamma-aminobutyric acid type B (GABAB) receptor-mediated inhibition of excitatory synaptic transmission and of action potential-evoked calcium currents were studied in hippocampal neurons in vitro with step-like changes of a saturating baclofen concentration. Inhibition mediated by postsynaptic GABAB receptors was excluded pharmacologically. Both presynaptic inhibition and reduction of calcium currents developed and declined exponentially with similar time constants of about 0.2 and 3 s, respectively. The close correlation of the time courses indicates that fast, G protein-mediated depression of voltage-gated calcium channels and thus direct reduction of the presynaptic calcium influx may contribute to the GABAB receptor-induced inhibition of excitatory synaptic transmission in hippocampal neurons in vitro.
利用饱和浓度巴氯芬的阶跃变化,在体外海马神经元中研究了γ-氨基丁酸B型(GABAB)受体介导的兴奋性突触传递抑制和动作电位诱发的钙电流的时间进程。通过药理学方法排除了突触后GABAB受体介导的抑制作用。突触前抑制和钙电流的减少均呈指数发展和衰减,其时间常数分别约为0.2秒和3秒。时间进程的密切相关性表明,快速的、G蛋白介导的电压门控钙通道抑制,以及由此导致的突触前钙内流直接减少,可能有助于体外海马神经元中GABAB受体诱导的兴奋性突触传递抑制。