Abstract
Cocaine, as an indirect dopamine agonist, induces selective behavioral and physiological events such as hyperlocomotion and dopamine release. These changes are considered as consequences of cocaine-induced molecular adaptation such as CREB and c-Fos. Recently, methanolic extracts from licorice was reported to decrease cocaine-induced dopamine release and c-Fos expression in the nucleus accumbens. In the present study, we investigated the effects of liquiritigenin (LQ), a main compound of licorice, on acute cocaine-induced behavioral and molecular changes in rats. LQ attenuated acute cocaine-induced hyperlocomotion in dose-dependent manner. In addition, LQ inhibited CREB phosphorylation and c-Fos expression in the striatum and the nucleus accumbens induced by acute cocaine. Results provide strong evidence that LQ effectively attenuates the acute behavioral effects of cocaine exposure and prevents the induction of selective neuroadaptive changes in dopaminergic signaling pathways. Further investigation of LQ from licorice extract might provide a novel therapeutic strategy for the treatment of cocaine addiction.
Highlights
Cocaine has been known as an indirect dopamine agonist to inhibit dopamine reuptake
To identify the involvement of molecular change in the mesolimbic dopamine system in the inhibition of hyperlocomotion by LQ, we examined the effect of LQ on the alteration of c-Fos expression and cAMP response elements binding (CREB) activation in the striatum and the nucleus accumbens induced by acute cocaine in separate groups of rats
Accumulating evidence has established that a single cocaine administration induces rapidly and transiently expresses c-Fos via CREB activation at the postsynaptic dopaminergic area
Summary
Cocaine has been known as an indirect dopamine agonist to inhibit dopamine reuptake It causes the release of dopamine in synaptic area of the mesolimbic and nigrostriatal DA system as a major mediator in the behavioral and reinforcing effects of cocaine [1]. C-Fos is a transcription factor which is one of the immediate early markers produced by acute cocaine. It is rapidly and transiently up-regulated for postsynaptic activation in dopaminergic target area including the striatum and the nucleus accumbens following acute cocaine [4]. In cocaine-treated brain, the expression of c-Fos is modulated by the activation of cAMP response elements binding (CREB). Acute cocaine administration induces the phosphorylation of CREB, which in turn leads to the expression of immediate early marker, c-Fos [5].
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