Somatostatin depresses excitability in neurons of the solitary tract complex through hyperpolarization and augmentation of IM, a non-inactivating voltage-dependent outward current blocked by muscarinic agonists.
Somatostatin depresses excitability in neurons of the solitary tract complex through hyperpolarization and augmentation of IM, a non-inactivating voltage-dependent outward current blocked by muscarinic agonists.
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生长抑素通过超极化和增强IM（一种被毒蕈碱激动剂阻断的非失活电压依赖性外向电流）来抑制孤束复合体神经元的兴奋性。
DOI：
10.1073/pnas.85.3.948
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发表时间：
1988
影响因子：
11.1
通讯作者：
Siggins,GR
中科院分区：
文献类型：
--
作者：
Jacquin,T;Champagnat,J;Madamba,S;Denavit-Saubié,M;Siggins,GR
含有生长抑素的纤维在神经系统中的突触功能存在争议。因此，我们用大鼠脑干切片的制备方法，测试了前生长抑素衍生肽对含有大量生长抑素纤维和胞体的孤束复合体神经元的电生理效应。灌流生长抑素-14和生长抑素-28(生长抑素-14的前体)，但不灌流生长抑素-28-(1-12)或-(1-10)，主要抑制自发的棘波和阈值下(可能是突触)活动。在细胞内记录中，生长抑素-14和-28使大多数神经元超极化，并伴随着轻微的(10-35%)但可重复的输入阻力下降。这些超极化反应在去极化的细胞中增强，并持续存在于氯注入后自发抑制性突触后电位变为去极化的细胞中。这些数据表明，生长抑素受体调节K+电导。在电压钳研究中，生长抑素-28和-14诱导了稳定的外向电流，并增强了电压依赖的、非激活的外向钾电导(IM)，这种外向K+电导被M胆碱能受体的激活所阻断。这些结果提示：(1)孤束复合体中含有生长抑素的成分可能通过激活突触后对钾离子的通透性而发挥抑制作用；(2)同一离子通道类型可能受两种神经递质--生长抑素和乙酰胆碱通过相互控制机制的共同调节。
The synaptic function of somatostatin-containing fibers in the nervous system is controversial. Therefore, we used a slice preparation of the rat brain stem to test the electrophysiological effects of prosomatostatin-derived peptides on neurons of the solitary tract complex, which contains an abundance of somatostatin-containing fibers and cell bodies. Superfusion of both somatostatin-14 and somatostatin-28 (the precursor for somatostatin-14), but not somatostatin-28-(1-12) or -(1-10), predominantly inhibited spontaneous spike and subthreshold (probably synaptic) activity. In intracellular recordings, somatostatin-14 and -28 hyperpolarized most neurons in association with a slight (10-35%) but reproducible decrease in input resistance. These hyperpolarizing responses were augmented in depolarized cells and persisted in cells in which spontaneous inhibitory postsynaptic potentials became depolarizing after Cl- injection. These data suggest that somatostatin receptors regulate a K+ conductance. In voltage-clamp studies, somatostatin-28 and -14 induced a steady outward current and augmented the voltage-dependent, nonactivating outward K+ conductance (IM) shown to be blocked by activation of muscarinic cholinergic receptors. These results suggest (i) that somatostatin-containing elements in the solitary tract complex play an inhibitory role through the activation of postsynaptic permeability to potassium ions and (ii) that the same ion channel type may be coregulated by two neurotransmitter candidates, somatostatin and acetylcholine, through a reciprocal control mechanism.