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PubMed · 7024401

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

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

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AnimalsCarboxy-LyasesCorpus StriatumDenervationFemaleGlutamate DecarboxylaseImmunoenzyme TechniquesKainic AcidNeuronsRatsSubstantia NigraJournal ArticleResearch Support, Non-U.S. Gov't

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W H Oertel, D E Schmechel, M J Brownstein, M L Tappaz, D H Ransom, I J Kopin. 1981. Decrease of glutamate decarboxylase (GAD)-immunoreactive nerve terminals in the substantia nigra after kainic acid lesion of the striatum.. https://doi.org/10.1177/29.8.7024401

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