Mediation by the corticostriatal input of the in vivo increase in rat striatal acetylcholine content induced by 2-chloroadenosine

Electrophysiological and biochemical studies have given evidence for the existence of a corticostriatal pathway in which glutamate may be the excitatory neurotransmitter. This pathway appears to innervate cholinergic neurons intrinsic to the striatum and to regulate their activity as the following results indicate: cholinergic interneurons are destroyed by the intrastriatal application of the neurotoxin, kainic acid, a conformationally restricted analog of glutamic acid and, cholinergic neurotransmission is compromised after long-term decortication, i.e., the acetylcholine turnover rate is decreased, the sodium-dependent high affinity uptake of choline is reduced and the muscarinic action of oxotremorine in increasing striatal acetylcholine content is prevented. Research outlined in the present communication demonstrates that the corticostriatal pathway mediates the depressant effect exerted by 2-chloroadenosine on striatal cholineric interneurons. This result is suggestive of an indirect action of the putative adenosine receptor agonist on striatal cholinergic neurotransmission.