Partial protection by CDP-choline against kainic acid-induced lesion in the rat caudate nucleus.
The acute intraperitoneal administration of CDP-choline to rats caused an increase in striatal dopamine (DA) synthesis, measured by DOPA accumulation after decarboxylase inhibition. Moreover, the chronic treatment with CDP-choline induced a decrease in the total number of 3H-spiroperidol binding sites, while partially antagonizing the disappearance of DA-sensitive adenylate cyclase activity elicited by intrastriatal kainic acid. These results suggest that CDP-choline may have a trophic and/or stimulant action on the function of nigrostriatal dopaminergic neurons.
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D002421:Caudate Nucleus / Q000187:drug effects* / Q000378:metabolism; D002794:Choline / Q000031:analogs & derivatives*; D003566:Cytidine Diphosphate Choline / Q000494:pharmacology*; D004298:Dopamine / Q000378:metabolism; D007608:Kainic Acid / Q000037:antagonists & inhibitors* / Q000633:toxicity; D007980:Levodopa / Q000378:metabolism; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects; D013134:Spiperone / Q000378:metabolism; D013997:Time Factors
D011954:Receptors, Dopamine; D015102:3,4-Dihydroxyphenylacetic Acid; D007980:Levodopa; D013134:Spiperone; D003566:Cytidine Diphosphate Choline; D002794:Choline; D007608:Kainic Acid; D004298:Dopamine