Maternal sleep deprivation affects extinction and reinstatement of methamphetamine reward memory in male offspring: Role of the D1-like and D2-like dopamine receptors.

Maternal sleep-deprivation (MSD) has been shown to induce stress, hyperactivity, and risk taking behavior in the offspring; howbeit, it is not yet clear whether it may also affect vulnerability to psychostimulant abuse in the offspring. We aimed to determine whether MSD affects extinction and reinstatement of methamphetamine (METH) reward memory in the offspring and also to evaluate the possible role of dopamine D1-like and D2-like receptors in these processes. Thirty-day-old male offspring born to control and sleep-deprived dams (during the third week of pregnancy) were trained to acquire METH-induced place preference (2 mg/kg., i.p.). METH reward memory was then reinstated following an 8-day period of extinction. The offspring received SCH 23390 (0.03 or 0.1 mg/kg, i.p.) or sulpiride (20 or 60 mg/kg, i.p.) as antagonists of dopamine D1-like and D2-like receptors, respectively, either immediately after each daily extinction session or prior to the reinstatement session. MSD postponed METH extinction and facilitated METH reinstatement in the offspring. SCH 23390 facilitated METH extinction and decreased reinstatement of the extinguished METH preference. Sulpiride in the offspring from sleep-deprived dams facilitated METH extinction, but it did not affect reinstatement of the extinguished METH reward memory. It seems that MSD may enhance vulnerability to METH abuse in the offspring. Furthermore, both dopamine D1-like and D2-like receptors may mediate METH extinction in the offspring born to the sleep-deprived dams; however, only the dopamine D1 receptor may play an important role in reinstating the extinguished METH reward memory in the offspring.