Naloxone enhances the release of acetylcholine from cholinergic interneurons of the striatum if the dopaminergic input is impaired.
Naloxone significantly enhanced the release of radioactive acetylcholine ([3H]ACh) from rat striatal slices loaded with [3H]choline either when the nigrostriatal pathway had been destroyed by 6-hydroxydopamine or when the D2 dopamine receptors had been inhibited by sulpiride. This in vitro study supplies the first neurochemical evidence, that, in addition to D2-receptor-mediated dopaminergic tonic control, there is opiate-receptor mediated presynaptic modulation of striatal ACh release, possibly by endogenous enkephalin released from local neurons. Such modulation occurs under conditions in which the dopaminergic input is impaired.
Sándor
N T
NT
Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
Kiss
J
J
Sándor
A
A
Lendvai
B
B
Vizi
E S
ES
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D002552:Cerebral Ventricles / Q000187:drug effects / Q000502:physiology*; D003342:Corpus Striatum / Q000187:drug effects / Q000502:physiology*; D004298:Dopamine / Q000502:physiology*; D007276:Injections, Intraventricular; D007395:Interneurons / Q000187:drug effects / Q000502:physiology*; D008297:Male; D009270:Naloxone / Q000494:pharmacology*; D009498:Neurotoxins / Q000494:pharmacology*; D016627:Oxidopamine / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D013469:Sulpiride / Q000494:pharmacology
D009498:Neurotoxins; D009270:Naloxone; D013469:Sulpiride; D016627:Oxidopamine; D001058:Apomorphine; D000109:Acetylcholine; D004298:Dopamine