Previous results from our lab showed that, the NMDA antagonist MK 801 abrogated the development and the expression of the stress-induced reinstatement (SR), in extinguished cocaine-induced conditioned place preference (CPP) rats, and that this was context-dependent and persistently observed on subsequent cocaine-induced reinstatements (CR). Our goal was to determine if a common glutamatergic mechanisms could be involved in the reconsolidation memory process on SR and CR.
Male Wistar rats (220-300g) were conditioned with cocaine (10-mg/kg ip) during four alternated drug/vehicle sessions and later extinguished with successive vehicle associations. The follow day, all groups of animal were reactivated in the CPP and immediately or 3 hs after the test injected with MK 801 (0.1 mg/kg ip) or vehicle, and 3 days after evaluated for a vehicle test. In the reinstatement day, 24 h after the vehicle test, a group of animals was 30 min-immobilized, and other the other group received a priming dose of cocaine (5 mg/kg) and were tested in the CPP. MK 801 administered immediately after the reactivation blocked both the SR and the CR, whereas the reinstatement showed up in both groups of animals injected 3 h after the reactivation.
The blockade of SR and CR by the NMDA antagonism immediately after the reactivation, could be attributed to a disruption of the reconsolidation memory process of the cocaine-induced CPP and the blockade of SR and CR support the hypothesis of a interchangeability of glutamatergic mechanism in the reinstatement of extinguished cocaine –induced conditioned palce preference rats.
