Decrease of glutamate decarboxylase (GAD)-immunoreactive nerve terminals in the substantia nigra after kainic acid lesion of the striatum.
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.
D000818:Animals; D002262:Carboxy-Lyases / Q000378:metabolism*; D003342:Corpus Striatum; D003714:Denervation; D005260:Female; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D007124:Immunoenzyme Techniques; D007608:Kainic Acid / Q000494:pharmacology; D009474:Neurons / Q000201:enzymology*; D051381:Rats; D013378:Substantia Nigra / Q000166:cytology / Q000201:enzymology*
D002262:Carboxy-Lyases; D005968:Glutamate Decarboxylase; D007608:Kainic Acid