Kainic acid-induced lesion of dopaminergic target cells in the striatum: consequences on the dynamics of cerebellar cGMP.
The bilateral intrastriatal injection of kainic acid (2 microgram/caudate) caused a marked decrease in the activity of striatal dopamine-sensitive adenylate cyclase. This probable loss of target cells for dopamine was associated with a parallel decrease of the cGMP level in the cerebellar cortex, which was maximal (80% loss) by 24 h and prevented apomorphine from raising cerebellar cGMP levels. On the contrary harmaline and isoniazid both increased the levels of cerebellar cGMP in kainic-lesioned rats to the same extent as in control rats. The results indicate that dopamine mechanisms in the striatum are involved in the regulation of cerebellar cortex cGMP.
D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D002525:Cerebellar Cortex / Q000378:metabolism; D002531:Cerebellum / Q000378:metabolism*; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism*; D004298:Dopamine / Q000502:physiology*; D006220:Haloperidol / Q000494:pharmacology; D006246:Harmaline / Q000494:pharmacology; D007538:Isoniazid / Q000494:pharmacology; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D011759:Pyrrolidines / Q000494:pharmacology*; D051381:Rats
D011759:Pyrrolidines; D006246:Harmaline; D000262:Adenylyl Cyclases; D006152:Cyclic GMP; D006220:Haloperidol; D001058:Apomorphine; D007608:Kainic Acid; D007538:Isoniazid; D004298:Dopamine