Sympathetic input to ganglia of the guinea pig sphincter of Oddi.
Sympathetic input to ganglia of the guinea pig sphincter of Oddi.
复制标题
豚鼠奥迪括约肌神经节的交感神经输入。
DOI：
10.1152/ajpgi.1994.266.6.g1162
复制
发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Mawe,GM
中科院分区：
文献类型：
--
作者：
Wells,DG;Mawe,GM
细胞内记录和免疫组织化学染色技术被用来建立是否括约肌的Oddi（SO）神经节是一个目标的交感神经输入到这个地区。去甲肾上腺素（0.01-10.0 μ M）降低刺激神经节间纤维束诱发的烟碱快速兴奋性突触后电位（EPSP）的幅度，半数最大抑制浓度（EC 50）为300 nM。去甲肾上腺素不改变神经元对乙酰胆碱的反应性。α 2-肾上腺素受体激动剂UK-14304模拟去甲肾上腺素诱导的效应，EC 50为2.5 nM，而α 1-和β-肾上腺素受体激动剂对EPSP无影响。α 2-肾上腺素受体拮抗剂idazoxan（1.0 μ M）抑制UK-14304反应，解离常数为1.0 nM。释放内源性的儿茶酚胺，通过添加酪胺（100 μ M）的浴，引起咪唑克生敏感的快速EPSP的幅度下降。在少数表现出抑制性突触后电位（IPSPs）的SO神经元中，去甲肾上腺素引起膜电位超极化。IPSP和去甲肾上腺素诱导的超极化被α 2-肾上腺素受体拮抗剂抑制。地昔帕明（1.0 μ M），一种摄取抑制剂，可逆地增加了IPSP的幅度。酪氨酸羟化酶和多巴胺β-羟化酶的免疫反应在SO神经节丛的神经纤维中共存，而在胞体中不存在。本研究结果表明，去甲肾上腺素作为抑制性神经递质在SO神经节的突触前和突触后活动。
Intracellular recording and immunohistochemical staining techniques were used to establish whether sphincter of Oddi (SO) ganglia are a target of sympathetic input to this region. Norepinephrine (0.01-10.0 microM) decreased the amplitude of the nicotinic fast excitatory postsynaptic potential (EPSP) evoked by stimulation of interganglionic fiber tracts, with a half-maximal inhibitory concentration (EC50) of 300 nM. Norepinephrine did not alter the responsiveness of the neurons to acetylcholine. The alpha 2-adrenoreceptor agonist UK-14304 mimicked the norepinephrine-induced effect with a EC50 of 2.5 nM, whereas alpha 1- and beta-adrenoreceptor agonists had no effect on the EPSP. The alpha 2-adrenoreceptor antagonist idazoxan (1.0 microM) inhibited the UK-14304 response, with a dissociation constant of 1.0 nM. Release of endogenous catecholamines, by the addition of tyramine (100 microM) to the bath, caused an idazoxan-sensitive decrease in the amplitude of the fast EPSP. In the minority of SO neurons that exhibited inhibitory postsynaptic potentials (IPSPs), norepinephrine caused a hyperpolarization of the membrane potential. The IPSP and the norepinephrine-induced hyperpolarization were inhibited by alpha 2-adrenoreceptor antagonists. Desipramine (1.0 microM), an uptake inhibitor, reversibly increased the amplitude of the IPSP. Immunoreactivities for tyrosine hydroxylase and dopamine beta-hydroxylase were coexistent in nerve fibers and nonexistent in cell bodies in the ganglionated plexus of the SO. The results of this study indicate that norepinephrine acts pre- and postsynaptically as an inhibitory neurotransmitter in SO ganglia.