INTRINSIC INHIBITION IN MAGNOCELLULAR NEUROENDOCRINE CELLS OF RAT HYPOTHALAMUS
INTRINSIC INHIBITION IN MAGNOCELLULAR NEUROENDOCRINE CELLS OF RAT HYPOTHALAMUS
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DOI：
10.1113/jphysiol.1984.sp015330
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发表时间：
1984-01-01
影响因子：
5.5
通讯作者：
DUDEK, FE
中科院分区：
文献类型：
--
作者：
ANDREW, RD;DUDEK, FE
通过大鼠下丘脑切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。超极化后电位（持续时间长达 125 毫秒）跟随单一动作电位，持续数百毫秒的后超极化 (a.h.p.) 跟随短暂的诱发尖峰序列。 a.h.p 的幅度和持续时间。在持续时间较长或频率较高的尖峰序列后增加。 a.h.p.似乎是内源性的，而不是由反复抑制引起的突触介导，因为它在轴突传导或化学突触传递的药理阻断后仍然存在。 a.h.p. 的逆转潜力。比抑制性突触后电位至少负20 mV。 Cl-离子导入法没有改变 a.h.p.细胞内 Ca2+ 与乙二醇 β-氨基乙醚 N,N,N''N''-四乙酸注射液的螯合消除了 a.h.p. Ca2+ 激活的 K+ 电导，而不是反复的突触抑制，显然导致了 a.h.p。并且至少部分地负责大细胞神经元单次尖峰后的抑制。在激素释放过程中，这种内源性机制可能有助于推定催产素能细胞的爆发后沉默期和阶段性神经元的爆发间期，已知这些神经元会激发与加压素释放相关的重复爆发。
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.) lasting hundreds of ms 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 ethylene glycol .beta.-aminoethyl ether N,N,N''N''-tetracetic acid 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 neurons, which are known to fire repetitive bursts associated with vasopressin release.