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树突毒素和4-氨基吡啶在低频电刺激期间增强神经垂体激素的分泌。

Dendrotoxin and 4-aminopyridine potentiate neurohypophysial hormone secretion during low frequency electrical stimulation.

作者信息

Bondy C A, Russell J T

机构信息

Laboratory of Neurochemistry, NINCDS, Bethesda, MD 20892.

出版信息

Brain Res. 1988 Jun 21;453(1-2):397-400. doi: 10.1016/0006-8993(88)90187-4.

Abstract

The K+ channel blockers dendrotoxin (10(-9) M) and 4-aminopyridine (10(-6) M) produce similar patterns of augmentation of electrically evoked vasopressin and oxytocin secretion from isolated rat neurointermediate lobes. Both channel blockers produced a greater than two-fold increase in vasopressin release. Oxytocin release, however, was comparably increased only when endogenous opioid inhibition was abolished by the presence of naloxone. The potentiation of hormone release was dependent on the frequency of the applied stimulus. A large effect was seen with 1000 pulses at 4 Hz but not when the same number of pulses was delivered at 12 Hz. These findings suggest that a specific type of K+-channel, sensitive to dendrotoxin and low micromolar 4-aminopyridine, may play a significant role in the frequency-dependent facilitation of secretion from neurohypophysial nerve endings.

摘要

钾离子通道阻滞剂树突毒素(10⁻⁹ M)和4-氨基吡啶(10⁻⁶ M)可使离体大鼠神经中间叶电诱发的血管加压素和催产素分泌产生相似的增强模式。两种通道阻滞剂均可使血管加压素释放增加两倍以上。然而,只有当纳洛酮消除内源性阿片类物质抑制作用时,催产素释放才会出现类似程度的增加。激素释放的增强取决于所施加刺激的频率。在4 Hz下施加1000个脉冲时可观察到显著效果,但在12 Hz下施加相同数量的脉冲时则未观察到。这些发现表明,一种对树突毒素和低微摩尔浓度的4-氨基吡啶敏感的特定类型钾离子通道,可能在神经垂体神经末梢分泌的频率依赖性促进过程中发挥重要作用。

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