Andrew R D, Dudek F E
J Physiol. 1984 Aug;353:171-85. doi: 10.1113/jphysiol.1984.sp015330.
Endogenous mechanisms of inhibition in magnocellular neuroendocrine cells were studied with intracellular recordings in the rat hypothalamic slice preparation. Hyperpolarizing after-potentials (duration up to 125 ms) followed single action potentials and after-hyperpolarizations (a.h.p.s) lasting hundreds of milliseconds followed brief evoked spike trains. The amplitude and duration of the a.h.p. increased after spike trains of longer duration or higher frequency. The a.h.p. appears endogenous, rather than synaptically mediated from recurrent inhibition, because it persisted after pharmacological blockade of axonal conduction or of chemical synaptic transmission. The reversal potential of the a.h.p. was at least 20 mV more negative than that of inhibitory post-synaptic potentials. Cl- ionophoresis did not alter the a.h.p. Chelation of intracellular Ca2+ with EGTA injection eliminated the a.h.p. A Ca2+-activated K+ conductance, rather than recurrent synaptic inhibition, apparently causes the a.h.p. and is at least partly responsible for the inhibition after single spikes in magnocellular neurones. During hormone release, this endogenous mechanism may contribute to the post-burst silent period in putative oxytocinergic cells and to the interburst interval in phasic neurones, which are known to fire repetitive bursts associated with vasopressin release.
利用大鼠下丘脑脑片制备中的细胞内记录，研究了大细胞神经内分泌细胞的内源性抑制机制。单个动作电位后跟随超极化后电位（持续时间长达125毫秒），短暂诱发的锋电位串后跟随持续数百毫秒的超极化后电位（a.h.p.s）。较长持续时间或较高频率的锋电位串后，a.h.p.的幅度和持续时间增加。a.h.p.似乎是内源性的，而非由折返抑制通过突触介导，因为在轴突传导或化学性突触传递被药物阻断后它仍然存在。a.h.p.的反转电位比抑制性突触后电位的反转电位至少负20 mV。Cl-离子透入不改变a.h.p.。注射EGTA螯合细胞内Ca2+消除了a.h.p.。一种Ca2+激活的K+电导，而非折返性突触抑制，显然引起了a.h.p.，并且至少部分负责大细胞神经元单个锋电位后的抑制。在激素释放期间，这种内源性机制可能促成假定的催产素能细胞中的爆发后静息期以及相位性神经元中的爆发间期，已知这些神经元会产生与血管加压素释放相关的重复性爆发。
