Historically, the suggestion that dopaminergic (DAergic) neurons are involved in the latent inhibition (LI) phenomenon is linked to psychopharmacological studies carried out by two laboratories reporting an attenuation of LI responses in animals (rats) treated with the indirect DAergic agonist d-amphetamine, after chronic (Solomon, Crider, Winkelman et al.,1981; Weiner, Lubow & Feldon, 1981, 1984) or acute administration (Weiner, Lubow & Feldon, 1988). Involvement of DAergic neurons in LI was further supported by data showing that the LI attenuation induced by d-amphetamine was reversed by the concomitant administration of the neuroleptic chlorpromazine (Solomon et al., 1981), and by subsequent studies showing a facilitation of LI expression after administration of haloperidol (Weiner & Feldon, 1987; Weiner, Feldon & Katz, 1987), a well-known typical neuroleptic with a potent blockade action on DA receptors. Since these first studies, the reversal of the d-amphetamine-induced LI reduction by DAergic antagonists has been found in different LI paradigms after administration of several atypical neuroleptics, including olanzapine (Gosselin, Oberling & Di Scala, 1996) and clozapine (Trimble, Bell & King, 1998; Russig, Murphy & Feldon, 2002). In other respects, enhancement of LI expression has also been reported, with the atypical antipsychotics displaying a selective blockade action on D2 receptors such as sulpiride (Feldon & Weiner, 1991) or remoxipride (Trimble, Bell & King, 1997), whereas selective D1 antagonists were found to have no effect on LI phenomenon (Trimble, Bell & King, 2002).