Chronic ganglioside treatment counteracts the biochemical signs of dopamine receptor supersensitivity induced by chronic haloperidol treatment.
Chronic ganglioside treatment (10 mg/kg, i.p.) using the molecular species with only one neuroaminic acid residue (GM1) given together with haloperidol (0.3 and 5 mg/kg, i.p.) once daily in male rats, counteracted the haloperidol-induced increase in the number of [3H]spiperone binding sites in striatal membranes when the low dose of haloperidol, but not the high dose, was administered. The present results therefore indicate that chronic GM1 treatment can partially counteract the increase in the number of dopamine receptors having a high affinity for neuroleptics (D2 type) induced by chronic haloperidol treatment in striatal membranes, and therefore may also partially counteract the development of neuroleptic-induced dopamine receptor supersensitivity.
D000818:Animals; D001665:Binding Sites / Q000187:drug effects; D003342:Corpus Striatum / Q000378:metabolism; D005732:Gangliosides / Q000008:administration & dosage* / Q000494:pharmacology; D006220:Haloperidol / Q000008:administration & dosage* / Q000494:pharmacology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000032:analysis / Q000187:drug effects*; D013134:Spiperone / Q000378:metabolism; D013997:Time Factors
D005732:Gangliosides; D011954:Receptors, Dopamine; C028051:neuroleptic receptor; D013134:Spiperone; D006220:Haloperidol