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美国耶鲁大学S.A.Tomiko等最近以电生理实验表明,GABA通过荷包牡丹碱(bicuculline,BC)-阻滞性受体,直接作用分离出的大鼠促黑激素(MSH)细胞,结果Cl~-电导增加,膜电位朝Cl~-平衡电位的方向发展,引起静息部位去极化或使高K~+诱发的去极化难以进行。作者发现GABA首先刺激MSH释放,尔后抑制之,同时抑制K~+诱发的MSH分泌。作者提供的药理学证据提示,上述分泌和电生理活动所涉及的受体相同。GABA能神经直接作用MSH细胞,改变其释放量,并受GABA产生的电生理特性的变化而影响其功能,这是GABA能神经功能的新发现。多采用大鼠为实验对象,先分离垂体后叶中间部细胞,体外短期培养,并置于柱形器皿内,持续灌流并测定MSH释放量。
Recently, SATomiko et al. From Yale University in the United States showed recently that electrophysiological experiments showed that GABA directly interacts with rat melanocyte (MSH) cells through bicuculline (BC) -receptor blocker. As a result, Cl ~ - conductance Increase, the membrane potential toward Cl ~ - potential balance direction, causing the rest part of the depolarization or high K ~ + induced depolarization difficult. The authors found that GABA first stimulated release of MSH, followed by inhibition, while inhibiting K ~ + -induced MSH secretion. The pharmacological evidence provided by the authors suggests that the above receptors for secretion and electrophysiological activity are the same. GABAergic nerve can directly affect MSH cells, change its release amount and influence its function by the change of electrophysiological characteristics produced by GABA, which is a new discovery of GABAergic nerve function. More rats were used as experimental subjects, the middle of the posterior pituitary cells were isolated first, cultured in vitro for short periods and placed in a cylindrical vessel for continuous perfusion and determination of MSH release.