Harrison N L, Lambert N A
Laboratory of Neurophysiology, National Institute for Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Neurosci Lett. 1989 Oct 23;105(1-2):137-42. doi: 10.1016/0304-3940(89)90025-6.
Chloride-dependent current responses to gamma-aminobutyric acid (GABA) were recorded from cultured rat hippocampal neurons under voltage clamp. In the presence of the membrane-permeable cyclic AMP analog, 8-bromo-cyclic AMP (8-Br-cAMP), the peak current response to GABA was reduced, although the reversal potential for the current evoked by GABA was unaltered; similar concentrations of 8-bromo-cyclic GMP did not alter the GABA response. 8-Br-cAMP also increased spontaneous activity of the neurons and blocked accommodation of firing. It is possible that the alterations in responses to GABA result from the activation of cyclic AMP-dependent protein kinase (cAMP-PK) and subsequent phosphorylation of the GABAA receptor.
在电压钳制条件下，记录培养的大鼠海马神经元对γ-氨基丁酸（GABA）的氯离子依赖性电流反应。在存在膜通透性环磷酸腺苷类似物8-溴环磷酸腺苷（8-Br-cAMP）的情况下，对GABA的峰值电流反应降低，尽管GABA诱发电流的反转电位未改变；类似浓度的8-溴环磷酸鸟苷不会改变GABA反应。8-Br-cAMP还增加了神经元的自发活动并阻断了放电适应。对GABA反应的改变可能是由于环磷酸腺苷依赖性蛋白激酶（cAMP-PK）的激活以及随后GABAA受体的磷酸化所致。
