Background and Purpose: Methamphetamine (METH) is a world-wide abused drug with no effective pharmacotherapy for its addiction available. Given the important role of sleep deprivation in increasing the risk of relapse to METH-seeking behavior, it is essential to investigate the mechanisms that could reduce the likelihood of relapse in drug users. Experimental Approach: Adolescent and adult male rats underwent chronic REM sleep deprivation (RSD) for 7 days. The rats were trained for a METH (2 mg/kg, i.p.) conditioned place preference (CPP). Thereafter, METH reward memory was retrieved during a reactivation session. Immediately after memory reactivation, the animals received the GABAB receptor agonist baclofen (0, 2.5 or 5 mg/kg, i.p.). Key Results: Results showed that baclofen, when given during the reconsolidation of a METH CPP, dose-dependently attenuated its reinstatement in adolescent and adult rats. RSD enhanced the CPP reinstatement in adolescent rats, but did not affect it in adults. While the attenuating dose-dependent effects of baclofen were preserved in the RSD adolescent rats, they were not observed anymore in sleep-deprived adults. Baclofen had no effects on GABAB-R1 subunit expression in the prefrontal cortex (PFC) of either adolescent or adult rats. RSD, however, enhanced GABAB-R1 subunit expression in the PFC, which was blocked dose-dependently by the baclofen treatment at both ages. Conclusion and Implications: These findings suggest an important role of the GABAB-R in METH memory reconsolidation at different ages, its vulnerability to RSD, and further support the use of baclofen as a phase-specific treatment option to reduce METH abuse related behaviors.