Levonantradol, a potent cannabinoid-related analgesic, antagonizes haloperidol-induced activation of striatal dopamine synthesis.
Levonantradol antagonized the compensatory acceleration of striatal dopamine synthesis induced by haloperidol. This effect was stereospecific, since the pharmacologically less active enantiomer, dextronantradol was approximately 30 times less effective. delta 9-Tetrahydrocannabinol at a dose 320 times higher than levonantradol also attenuated the haloperidol effect, but cannabidiol was inactive at a dose 750 times higher. GABA-like actions of levonantradol may be responsible for this responsible for this antagonism of haloperidol, but anticholinergic effects may also contribute.
D000700:Analgesics / Q000494:pharmacology*; D000818:Animals; D003342:Corpus Striatum / Q000378:metabolism; D004298:Dopamine / Q000096:biosynthesis*; D013759:Dronabinol / Q000494:pharmacology; D006220:Haloperidol / Q000037:antagonists & inhibitors*; D008297:Male; D010617:Phenanthridines / Q000494:pharmacology*; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects; D013237:Stereoisomerism; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D000700:Analgesics; D010617:Phenanthridines; D011954:Receptors, Dopamine; D005680:gamma-Aminobutyric Acid; D013759:Dronabinol; C025490:nantradol; D006220:Haloperidol; D004298:Dopamine