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纹状体经 kainic 酸损伤后黑质中谷氨酸脱羧酶(GAD)免疫反应性神经末梢减少。

Decrease of glutamate decarboxylase (GAD)-immunoreactive nerve terminals in the substantia nigra after kainic acid lesion of the striatum.

作者信息

Oertel W H, Schmechel D E, Brownstein M J, Tappaz M L, Ransom D H, Kopin I J

出版信息

J Histochem Cytochem. 1981 Aug;29(8):977-80. doi: 10.1177/29.8.7024401.

Abstract

Antiserum sheep 3 against rat brain glutamate decarboxylase (GAD) was employed for the immunohistochemical localization of GAD-immunoreactive nerve terminals in the substantia nigra (SN). To test whether the antiserum specifically localized GAD-containing axon terminals, the effect of kainic acid-induced striatal lesions on the reactive nerve endings in the SN was investigated. Seven days after the injection of 1 microgram kainic acid into the striatum, a 65% decrease in GAD-enzyme activity occurred in the ipsilateral SN. On immunohistochemical examination there was correspondingly a marked reduction of GAD-positive terminals. The parallel decrease in biochemical and immunohistochemical GAD activity indicates that antiserum sheep 3 can be used as a specific immunohistochemical probed for GAD-containing elements.

摘要

用抗大鼠脑谷氨酸脱羧酶(GAD)的羊抗血清3对黑质(SN)中GAD免疫反应性神经末梢进行免疫组织化学定位。为了检测该抗血清是否能特异性定位含GAD的轴突终末,研究了海人酸诱导的纹状体损伤对SN中反应性神经末梢的影响。向纹状体注射1微克海人酸7天后,同侧SN中GAD酶活性降低了65%。免疫组织化学检查相应地显示GAD阳性终末显著减少。生化和免疫组织化学GAD活性的平行降低表明羊抗血清3可作为检测含GAD成分的特异性免疫组织化学探针。

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