N-methyl d-aspartate receptors are involved in the induction, but not expression stage of amphetamine sensitization in schedule-induced polydipsia in rats.

1. The aim of the present study was to examine the role of dopaminergic and glutamatergic receptors on different stages of the amphetamine (AMPH) sensitized effect in schedule-induced polydipsia (SIP) in rats. 2. Three experiments were designed to evaluate the roles of DAD2 receptor antagonist haloperidol (HAL) and glutamatergic N-methyl d-aspartate receptor antagonist MK-801 on both the induction and the expression stage of AMPH sensitization in SIP rats. First, the induction of AMPH sensitization in the SIP model was tested again to confirm previous findings. Second, HAL or MK-801 was co-administered with AMPH on five consecutive days and their effect on induction was examined 14 days after withdrawal. Finally, HAL or MK-801 was co-administered with AMPH on the final day of testing in SIP rats in which AMPH sensitization had been established previously. 3. The present results showed that HAL and MK-801 affected the effect of AMPH differently during the process of sensitization. Whereas HAL influenced the sensitization during both the induction and the expression phases, MK-801 affected only the induction phase; thus, once the sensitization had been established, MK-801 had no further influence. 4. These results suggest that the SIP model could be considered useful for the study of sensitization. In addition, the induction and expression of AMPH sensitization is influenced differently by the dopaminergic and glutamatergic systems.