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

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.