Exogenous SO donor treatment impairs reconsolidation of drug reward memory in mice.

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.