The role of dopaminergic systems in γ-hydroxybutyrate-induced electrocorticogram hypersynchronization in the rat

Abstract

The effects of dopaminergic agonists and antagonists on the duration of hypersynchronization induced in the electrocorticogram (ecog) by γ-hydroxybutyrate (γ-HB) were tested in rats. Apomorphine (0·2–8 mg kg−1), piribedil (2·5–10 mg kg−1) and haloperidol (0·5–1 mg kg−1) had no influence on the duration of the hypersynchrony. Amphetamine (1·5–6 mg kg−1) inhibited the hypersynchrony, while (3,4-dihydroxyphenylamino)-2-imidazoline (DPI; 5, but not 1, mg kg−1) prolonged its duration. The lack of effect of the dopamine receptor agonists apomorphine and piribedil, and the dopamine receptor blocker haloperidol, on the γ-HB-induced hypersynchrony might indicate that the inhibition of the impulse flow in the nigrostriatal dopamine system by γ-HB is not involved in the generation of the hypersynchrony. DPI is thought to be an agonist at a dopamine receptor not sensitive to apomorphine, and its facilitatory effect on γ-HB-hypersynchrony can be interpreted in terms of a possible involvement of another dopamine system in the ecog hypersynchrony induced by γ-HB. The antagonism of γ-HB by amphetamine is possibly due to an indirect stimulatory effect on noradrenergic receptors.