Sleep Disorders Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Substance Abuse Prevention Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Brain Res. 2022 Oct 1;1792:148033. doi: 10.1016/j.brainres.2022.148033. Epub 2022 Jul 26.
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.
母体睡眠剥夺（MSD）已被证明会在后代中引起应激、多动和冒险行为；然而，目前尚不清楚它是否也会影响后代对精神兴奋剂滥用的易感性。我们旨在确定 MSD 是否会影响后代中甲基苯丙胺（METH）奖励记忆的消退和重新激活，以及评估多巴胺 D1 样和 D2 样受体在这些过程中的可能作用。来自对照组和睡眠剥夺组（在妊娠的第三周）的 30 天大雄性后代接受了 METH 诱导的位置偏好训练（2mg/kg，ip）。然后，在 8 天的消退期后，重新激活 METH 奖励记忆。后代接受了 SCH 23390（0.03 或 0.1mg/kg，ip）或舒必利（20 或 60mg/kg，ip），分别作为多巴胺 D1 样和 D2 样受体的拮抗剂，在每次每日消退后立即给予或在重新激活前给予。MSD 延迟了后代中 METH 的消退并促进了 METH 的重新激活。SCH 23390 促进了 METH 的消退并减少了消退的 METH 偏好的重新激活。舒必利在睡眠剥夺组的后代中促进了 METH 的消退，但不影响消退的 METH 奖励记忆的重新激活。似乎 MSD 可能会增加后代对 METH 滥用的易感性。此外，多巴胺 D1 样和 D2 样受体都可能介导来自睡眠剥夺的后代的 METH 消退；然而，只有多巴胺 D1 受体可能在重新激活消退的 METH 奖励记忆方面发挥重要作用。
