Kinetic analysis of GM1 effects on haloperidol-induced dopaminergic supersensitivity.

The relative affinity of metoclopramide as indicated by K(B) values was calculated in control and in haloperidol-withdrawn rats treated or not with monosialoganglioside-1 (GM1) by using dose-response curves constructed for apomorphine-induced stereotyped behavior. Haloperidol withdrawal decreased K(B) data--that is, increased the D2-receptor affinity for metoclopramide. GM1 treatment per se did not modify K(B) values but, when given in combination with haloperidol, GM1 induced a decrease in K(B) values. No differences were found in K(B) data when GM1 was administered after withdrawal from haloperidol.