Kaila K, Paalasmaa P, Taira T, Voipio J
Department of Zoology, University of Helsinki, Finland.
Neuroreport. 1992 Jan;3(1):105-8. doi: 10.1097/00001756-199201000-00028.
Extracellular pH transients were evoked in rat hippocampal brain slices by activation of a monosynaptic inhibitory pathway following pharmacological blockade of glutaminergic transmission. Repetitive stimulation in stratum radiatum near the recording site in stratum pyramidale evoked an immediate alkaline shift which was potentiated by pentobarbital and blocked by picrotoxin but not by 2-hydroxy-saclofen. Benzolamide, a poorly permeant inhibitor of carbonic anhydrase (CA), and prontosil-dextran 5000, a macromolecular CA inhibitor, abolished the alkaline transients evoked by stimulation and by exogenous GABA. Thus an extracellular CA is involved in regulating interstitial pH in brain, and the stimulation-induced alkaline transients are caused by net influx of CO2 into CA1 neurons in response to efflux of bicarbonate across postsynaptic GABAA receptor channels.
在对谷氨能传递进行药理学阻断后，通过激活单突触抑制通路在大鼠海马脑片中诱发细胞外pH瞬变。在锥体层记录部位附近的辐射层进行重复刺激，诱发了立即的碱化转变，戊巴比妥可增强该转变，而苦味毒可阻断该转变，但2-羟基-舒氯芬不能阻断。苯甲酰胺是一种渗透性较差的碳酸酐酶（CA）抑制剂，而百浪多息-葡聚糖5000是一种大分子CA抑制剂，它们消除了刺激和外源性GABA诱发的碱化瞬变。因此，细胞外CA参与调节脑内的间质pH，刺激诱导的碱化瞬变是由于二氧化碳响应于碳酸氢盐通过突触后GABAA受体通道外流而净流入CA1神经元所致。
