Key Laboratory of Molecular Epidemiology of Hunan Province, School of Medicine, Hunan Normal University, Changsha, 410081, China; Neuroscience Research Center, Institute of Medical and Health Science of HeBMU, Hebei Medical University, Shijiazhuang, 050017, China.
Neuroscience Research Center, Institute of Medical and Health Science of HeBMU, Hebei Medical University, Shijiazhuang, 050017, China.
Eur J Pharmacol. 2021 Apr 5;896:173911. doi: 10.1016/j.ejphar.2021.173911. Epub 2021 Jan 24.
Substance-related and addictive disorders (SRADs) are characterized by compulsive drug use and recurrent relapse. The persistence of pathological drug-related memories indisputably contributes to a high propensity to relapse. Hence, strategies to disrupt reconsolidation of drug reward memory are currently being pursued as potential anti-relapse interventions. Sulfur dioxide (SO), acting as a potential gaseous molecule, endogenously derives from sulfur amino acid and can exert significant neural regulatory effects. However, the role of SO in reconsolidation of drug memory has not been determined. In the present study, we used morphine- or cocaine-induced conditioned place preference (CPP) mouse models with retrieval to investigate the effects of exogenous SO donor treatment on reconsolidation of drug reward memory. We found that administration of SO donor immediately after the retrieval impaired the expression of morphine or cocaine CPP. Furthermore, the exogenous SO donor treatment 6 h post-retrieval or in the absence of retrieval had no effect on drug reward memory and the expression of CPP. SO itself did not produce aversive effects nor did it acutely block morphine CPP. Our results indicate that exogenous SO impairs reconsolidation of drug reward memory rather than inhibits the expression of drug reward memory. As such, SO2 holds potential for the treatment and prevention of SRADs and should be studied further.
物质相关和成瘾障碍（SRADs）的特征是强迫性药物使用和反复复发。病理性药物相关记忆的持续存在无疑增加了复发的倾向。因此，目前正在寻求破坏药物奖励记忆再巩固的策略，作为潜在的抗复发干预措施。二氧化硫（SO）作为一种潜在的气体分子，来源于含硫氨基酸，可发挥重要的神经调节作用。然而，SO 在药物记忆再巩固中的作用尚未确定。在本研究中，我们使用吗啡或可卡因诱导的条件位置偏好（CPP）小鼠模型进行检索，以研究外源性 SO 供体处理对药物奖赏记忆再巩固的影响。我们发现，在检索后立即给予 SO 供体处理会损害吗啡或可卡因 CPP 的表达。此外，在外源 SO 供体处理后 6 小时或在没有检索的情况下进行处理，对药物奖赏记忆和 CPP 的表达没有影响。SO 本身不会产生厌恶效应，也不会急性阻断吗啡 CPP。我们的结果表明，外源性 SO 损害药物奖赏记忆的再巩固，而不是抑制药物奖赏记忆的表达。因此，SO2 有可能用于治疗和预防 SRADs，应进一步研究。
