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脑干γ-氨基丁酸能神经回路对下行性抗伤害感受控制的作用:II. 大鼠中脑导水管周围灰质向中缝大核投射的γ-氨基丁酸能控制的电子显微镜免疫细胞化学证据

Contribution of brainstem GABAergic circuitry to descending antinociceptive controls: II. Electron microscopic immunocytochemical evidence of GABAergic control over the projection from the periaqueductal gray to the nucleus raphe magnus in the rat.

作者信息

Reichling D B, Basbaum A I

机构信息

Department of Neuroscience, University of California, San Francisco 94143.

出版信息

J Comp Neurol. 1990 Dec 8;302(2):378-93. doi: 10.1002/cne.903020214.

Abstract

Pharmacological, physiological, and behavioral studies suggest that inhibitory GABAergic neurons influence the projection from the midbrain periaqueductal gray matter to the medullary nucleus raphe magnus. The present study used electron microscopic immunocytochemical techniques to examine the morphology and synaptic relationships of GABA-immunoreactive terminals in the ventrolateral periaqueductal gray. These putative GABAergic terminals comprise almost 40% of all axon terminals in the periaqueductal gray. GABA-immunoreactive terminals contain small, clear, pleomorphic or round, vesicles, and 46% also contain some dense-cored vesicles. In some experiments we also used a colloidal gold-conjugated retrograde tracer to label periaqueductal gray neurons that project to the nucleus raphe magnus. About half of the synaptic inputs onto the cell bodies and proximal dendrites of retrogradely labeled neurons are GABA-immunoreactive; these putative GABAergic synapses, which directly control activity in neurons projecting from the periaqueductal gray to the nucleus raphe magnus, might mediate the antinociception-related effects of exogenous GABAA receptor ligands.

摘要

药理学、生理学和行为学研究表明,抑制性γ-氨基丁酸能神经元会影响从中脑导水管周围灰质到延髓中缝大核的投射。本研究采用电子显微镜免疫细胞化学技术,研究腹外侧导水管周围灰质中γ-氨基丁酸免疫反应性终末的形态和突触关系。这些假定的γ-氨基丁酸能终末几乎占导水管周围灰质中所有轴突终末的40%。γ-氨基丁酸免疫反应性终末含有小的、清亮的、多形性或圆形的囊泡,46%的终末还含有一些致密核心囊泡。在一些实验中,我们还使用了胶体金结合的逆行示踪剂来标记投射到中缝大核的导水管周围灰质神经元。逆行标记神经元的胞体和近端树突上约一半的突触输入是γ-氨基丁酸免疫反应性的;这些假定的γ-氨基丁酸能突触直接控制从导水管周围灰质投射到中缝大核的神经元的活动,可能介导外源性γ-氨基丁酸A受体配体的抗伤害感受相关作用。

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