Bourque C W, Brown D A
M.R.C. Neuropharmacology Research Group, School of Pharmacy, University of London, U.K.
Neurosci Lett. 1987 Nov 23;82(2):185-90. doi: 10.1016/0304-3940(87)90127-3.
Magnocellular neurosecretory cells (MNCs) were impaled in perfused explants of rat hypothalamus. Evoked bursts of spikes were followed by an afterhyperpolarization (AHP) lasting 1-2 s. In each of 22 cells this AHP was selectively suppressed by low nanomolar concentrations of apamin (IC50 = 1.3 nM) or micromolar concentrations of d-tubocurarine (IC50 approximately 40 microM). Blockade of the AHP was accompanied by a decrease in spike accommodation and an unmasking of the late depolarizing afterpotential which induces burst firing in MNCs. Modulation of the Ca2+-dependent K+ (AHP) conductance by an endogenous apamin-like ligand could play an important role in the control of firing rate and pattern in MNCs.
在大鼠下丘脑灌流外植体中刺入大细胞神经分泌细胞(MNCs)。诱发的一串动作电位之后是持续1 - 2秒的超极化后电位(AHP)。在22个细胞中的每一个中,这种AHP被低纳摩尔浓度的蜂毒明肽(IC50 = 1.3 nM)或微摩尔浓度的d -筒箭毒碱(IC50约为40 microM)选择性抑制。AHP的阻断伴随着动作电位适应的减少以及晚期去极化后电位的暴露,晚期去极化后电位可诱发MNCs的爆发式放电。内源性蜂毒明肽样配体对Ca2 +依赖性K +(AHP)电导的调节可能在MNCs放电频率和模式的控制中起重要作用。