Abstract
Relapse to drug seeking after prolonged abstinence is a major problem in the clinical treatment of drug addiction. The use of pharmacological interventions to disrupt established drug reward memories is a promising strategy for the treatment of drug addiction. A growth hormone secretagogue receptor 1 A antagonist, JMV2959, has been shown to reduce morphine-induced conditioned place preference (CPP) in rats within hours of intervention; thus, JMV2959 is a potential candidate for drug addiction treatment. However, the effect of JMV2959 on reconsolidation to disrupt drug seeking remains unknown. In this study, we assessed the effect of JMV2959 on morphine induced memory reconsolidation to inhibit drug seeking after drug withdrawal. Our results showed that the administration of JMV2959 (6 mg/kg) significantly reduced environmental cue induced CPP, which suggested a preventive effect of JMV2959 on morphine induced memory reconsolidation. Additionally, JMV2959 administration significantly altered the locomotor activity and food and water intake but did not significantly alter the natural reward preference. We concluded that JMV2959 may be an effective candidate to treat drug addiction.
Highlights
Drug addiction is a chronic relapsing brain disorder that is often caused by the persistent intake of morphine, cocaine, amphetamine, or fentanyl over a long period (Leshner, 1997; O’Brien and McLellan, 1996)
Our results showed that the administration of JMV2959 (6 mg/kg) significantly reduced environmental cue induced conditioned place preference (CPP), which suggested a preventive effect of JMV2959 on morphine induced memory reconsolidation
Two-way repeated-measures analysis of variance (ANOVA) analyse indicated that there was significant difference between the group exposed to JMV2959 (6 mg/kg) and the saline group(ANOVA, F(1,15) 45.46, p < 0.01), which indicated that JMV2959 was able to influence the locomotor activity of the rats and that the CPP score was valid (Figure 2)
Summary
Drug addiction is a chronic relapsing brain disorder that is often caused by the persistent intake of morphine, cocaine, amphetamine, or fentanyl over a long period (Leshner, 1997; O’Brien and McLellan, 1996). These addictive drugs activate human neurological systems through neurotrophic factors to form drug reward memory. This newly learned memory can be transformed into stable memories via memory consolidation (Davis and Squire, 1984; McGaugh, 2000) When this stabilised drug memory is recalled or reactivated, it undergoes additional consolidation, known as reconsolidation. The reconsolidated drug reward memory is labile and sensitive to certain disruptors, such as receptor antagonists, pharmacological techniques, and protein synthesis inhibitors
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