Reduction of nigral glutamic acid decarboxylase in rats with neuroleptic-induced oral dyskinesia.
Following eight monthly haloperidol decanoate injections rats showed an increased rate of vacuous chewing movements (VCM's), which gradually disappeared within 4 drug-free months. Another single dose of non-decanoate haloperidol reinstated a second increase in VCM rate which was still significant after 2 months. The glutamic acid decarboxylase (GAD) activity in the substantia nigra of these chronically haloperidol-treated rats was lower than untreated controls. Furthermore, there was a significant negative correlation between individual VCM rates and nigral GAD activity. No corresponding changes occurred in other brain regions. The depression of nigral GAD may reflect a reduced tissue density of GABA-ergic axon terminals within the descending striato-nigral pathway.
D000818:Animals; D014150:Antipsychotic Agents / Q000494:pharmacology*; D004409:Dyskinesia, Drug-Induced / Q000201:enzymology*; D005260:Female; D005968:Glutamate Decarboxylase / Q000037:antagonists & inhibitors*; D006220:Haloperidol / Q000494:pharmacology; D009059:Mouth Diseases / Q000139:chemically induced; D051381:Rats; D011919:Rats, Inbred Strains; D013378:Substantia Nigra / Q000201:enzymology*
D014150:Antipsychotic Agents; D005968:Glutamate Decarboxylase; D006220:Haloperidol