MODULATION OF TRANSMITTER RELEASE FROM THE TERMINALS OF THE LOCUST WING STRETCH-RECEPTOR NEURON BY MUSCARINIC ANTAGONISTS
MODULATION OF TRANSMITTER RELEASE FROM THE TERMINALS OF THE LOCUST WING STRETCH-RECEPTOR NEURON BY MUSCARINIC ANTAGONISTS
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DOI：
10.1002/neu.480280406
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发表时间：
1995-12-01
期刊：
影响因子：
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通讯作者：
PITMAN, RM
中科院分区：
文献类型：
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作者：
LEITCH, B;PITMAN, RM
前翅牵张感受器（SR）神经元与降翅运动神经元建立单突触连接；在这篇文章中，对其输出到第一基底运动神经元（BA1）的药理学进行了研究。SR 与迄今为止研究的其他昆虫传入神经一样，似乎是胆碱能的；烟碱拮抗剂镓胺 (10(-4) M) 可逆地抑制传递，而 α-银环蛇毒素 (10(-6) M) 则不可逆地抑制传递，胆碱再摄取阻滞剂 hemicholinium-3 (10(-4) M) 也会导致 BA1 中记录的 SR 兴奋性突触后电位 (EPSP) 振幅可逆性降低，受体 亚型非选择性毒蕈碱拮抗剂阿托品 (10(-4) M)、东莨菪碱 (10(-4) M) 和苯甲酸奎宁环酯 (10(-5) M) 与烟碱拮抗剂不同，会导致 EPSP 振幅增强。这种效应似乎不是由运动神经元对乙酰胆碱 (ACh) 敏感性增加引起的，因为 阿托品对施加到 BA1 体的 ACh 压力的反应幅度产生显着降低而不是增加，东莨菪碱仅引起 ACh 体反应幅度的适度降低，对这些观察结果的最简单解释是，毒蕈碱拮抗剂通过阻断通常下调 ACh 释放的突触前自身受体，导致 EPSP 幅度增加。 SR 端子。毒蕈碱受体亚型选择性拮抗剂的作用表明，该制剂中的突触前受体可能具有与脊椎动物 M(2) 受体比 M(1) 或 M(3) 亚型更相似的药理学特征。讨论了该制剂中自身受体的功能意义。 (C) 1995 约翰威利父子公司
The forewing stretch receptor (SR) neuron makes monosynaptic connections with wing depressor motoneurons; in this article the pharmacology of its output onto the first basalar motoneuron (BA1) has been investigated, The SR, like other insect afferents that have been studied so far, appears to be cholinergic; transmission was suppressed reversibly by the nicotinic antagonist gallamine (10(-4) M) and irreversibly by alpha-bungarotoxin( 10(-6) M), The choline reuptake blocker hemicholinium-3 (10(-4) M) also caused a reversible reduction in the amplitude of SR excitatory postsynaptic potentials( EPSPs) recorded in BA1, The receptor subtype nonselective muscarinic antagonists atropine (10(-4) M), scopolamine (10(-4) M), and quinuclidinyl benzilate (10(-5) M), unlike nicotinic antagonists, caused an augmentation in EPSP amplitude, This effect does not appear to be caused by an increase in sensitivity of the motoneuron to acetylcholine (ACh), since atropine produced a marked reduction rather than an increase in the amplitude of responses to ACh pressure applied to the soma of BA1, Scopolamine only caused a modest reduction in the amplitude of ACh somatic responses, The simplest explanation for these observations is that muscarinic antagonists bring about an increase in EPSP amplitude by blockade of presynaptic autoreceptors that normally down-regulate the release of ACh from SR terminals. The effects of muscarinic receptor subtype-selective antagonists indicate that presynaptic receptors in this preparation may have a pharmacological profile more similar to that of vertebrate M(2) receptors than to that of M(1), or M(3) subtypes, The functional significance of autoreceptors in this preparation are discussed. (C) 1995 John Wiley & Sons, Inc.