Striatal cholinergic receptors and dyskinetic motor activity in the rat.
An injection of D-tubocurarine into the rat striatum produces a complex motor syndrome resembling in part that induced by picrotoxin. The destruction of the dopaminergic terminals by 6-hydroxydopamine does not prevent these effects of D-tubocurarine on motor activity. Hence neither dopamine release nor the presynaptic acetylcholine receptors are responsible for the D-tubocurarine-induced movements. On the other hand, lesion of the striatum by kainic acid abolishes the motor abnormalities due to D-tubocurarine but not those due to picrotoxin injection. Therefore, the effects of picrotoxin might be attributable to an action on GABA receptors still present in the kainic acid-treated striatum, whereas the effects of D-tubocurarine might be due to its action on striatal postsynaptic acetylcholine receptors.
D000818:Animals; D003342:Corpus Striatum / Q000187:drug effects / Q000503:physiopathology*; D004298:Dopamine / Q000378:metabolism; D006892:Hydroxydopamines / Q000494:pharmacology; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D009069:Movement Disorders / Q000503:physiopathology*; D009434:Neural Pathways / Q000503:physiopathology; D010852:Picrotoxin / Q000494:pharmacology; D051381:Rats; D011950:Receptors, Cholinergic / Q000502:physiology*; D013378:Substantia Nigra / Q000503:physiopathology; D014403:Tubocurarine / Q000494:pharmacology*
D004298:Dopamine; D006892:Hydroxydopamines; D007608:Kainic Acid; D010852:Picrotoxin; D011950:Receptors, Cholinergic; D014403:Tubocurarine