Abstract
Over the last decades, the endocannabinoid system has been implicated in a large variety of functions, including a crucial modulation of brain-reward circuits and the regulation of motivational processes. Importantly, behavioral studies have shown that cannabinoid compounds activate brain reward mechanisms and circuits in a similar manner to other drugs of abuse, such as nicotine, alcohol, cocaine, and heroin, although the conditions under which cannabinoids exert their rewarding effects may be more limited. Furthermore, there is evidence on the involvement of the endocannabinoid system in the regulation of cue- and drug-induced relapsing phenomena in animal models. The aim of this review is to briefly present the available data obtained using diverse behavioral experimental approaches in experimental animals, namely, the intracranial self-stimulation paradigm, the self-administration procedure, the conditioned place preference procedure, and the reinstatement of drug-seeking behavior procedure, to provide a comprehensive picture of the current status of what is known about the endocannabinoid system mechanisms that underlie modification of brain-reward processes. Emphasis is placed on the effects of cannabinoid 1 (CB1) receptor agonists, antagonists, and endocannabinoid modulators. Further, the role of CB1 receptors in reward processes is investigated through presentation of respective genetic ablation studies in mice. The vast majority of studies in the existing literature suggest that the endocannabinoid system plays a major role in modulating motivation and reward processes. However, much remains to be done before we fully understand these interactions. Further research in the future will shed more light on these processes and, thus, could lead to the development of potential pharmacotherapies designed to treat reward-dysfunction-related disorders.
Highlights
Cannabis is considered as one of the oldest and most widely used recreational drugs in the world
The intracranial administration of DHβE, an α4β2 nicotinic acetylcholine receptors (nAChRs) antagonist, but not MLA, an α7 nAChR antagonist, into each region blocked the AM251-induced attenuation of the reinstatement. These findings suggest that reinstatement to MAP-seeking behavior may be due to two steps: inhibition of ACh transmission by the activation of cannabinoid cannabinoid 1 (CB1) receptors and inactivation of α4β2 nAChRs [206]
CONCLUSION the euphorigenic properties of cannabis preparations have been appreciated by humans for centuries, only the last years we have acquired the experimental tools to evaluate cannabinoid reward and abuse liability in experimental animals
Summary
Cannabis is considered as one of the oldest and most widely used recreational drugs in the world. The attraction of cannabis and the many issues surrounding its illegality stem from its effects on sensory processing, euphoric sensations, and its relaxing inferences These effects are mainly attributed to the key psychoactive ingredient of marijuana, ∆9-tetrahydrocannabinol (∆9-THC) [5,6,7,8]. The discovery of the endogenous cannabinoid system has fueled the progressing amount of cannabinoid research in recent years, with particular emphasis on the effects of endogenous and synthetic cannabinoid compounds on cannabinoid 1 receptors (CB1 receptors) found in different areas of the brain This system is thought to modulate the motivational processes and rewardseeking behaviors associated with the use of cannabis. The present review summarizes recent animal studies that investigate the function of the endocannabinoid system and its involvement in brain-reward systems, with particular emphasis on the role of CB1 receptors
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