Thyrotropin-releasing hormone-immunoreactive nerve terminals synapse on the dendrites of gastric vagal motoneurons in the rat.
Thyrotropin-releasing hormone-immunoreactive nerve terminals synapse on the dendrites of gastric vagal motoneurons in the rat.
复制标题
大鼠胃迷走运动神经元树突上的促甲状腺素释放激素免疫反应性神经末梢突触。
DOI：
10.1002/cne.902940208
复制
发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Miselis,RR
中科院分区：
文献类型：
--
作者：
Rinaman,L;Miselis,RR
Thyrotropin‐releasing hormone stimulates vagally mediated gastric acid secretion and motility by an undefined central mechanism in the rat. The present study sought to determine the anatomical basis for this stimulatory effect by examining the ultrastructural relationship of nerve terminals immunoreactive for thyrotropin‐releasing hormone with the dendrites of gastric vagal motoneurons. A light and electron microscopic double immunostaining technique was employed using the beta subunit of unconjugated cholera toxin as a neural tracer. Cholera toxin (50 μl, 0.25%) was injected into the ventral stomach musculature in five rats. After 72 hours' survival, animals were sacrificed by transcardiac perfusion fixation. Retrogradely transported choleratoxin was immunocytochemically localized in vagal gastric motoneurons and their dendrites in the dorsal motor nucleus of the vagus and nucleus of the solitary tract, alone or in combination with the immunocytochemical localization of thyrotropin‐releasing hormone.Ultrastructural analysis of double‐labeled material revealed thyrotropin releasing hormone‐immunoreactive nerve terminals making asymmetric synaptic contacts on the retrogradely labeled dendrites of vagal gastric motoneurons. Nerve terminals immunoreactive for thyrotropin‐releasing hormone also made asymmetric and symmetric synaptic contacts with unlabeled dendrites of undetermined perikaryal origin. In addition, nonsynaptic varicosities immunoreactive for thyrotropin‐releasing hormone were frequently observed in the vagal nuclei. The synaptic contacts between thyrotropin‐releasing hormone‐immunoreactive nerve terminals and vagal gastric motoneuronal dendrites provide one possible basis for the profound stimulatory effect of central thyrotropin‐releasing hormone on gastric vagal motor activity.
