Abstract
The aim of this study was to evaluate changes in the expression of cannabinoid type 1 (CB1) and 2 (CB2) receptor proteins in several brain regions in rats undergoing cocaine self-administration and extinction training. We used a triad-yoked procedure to distinguish between the motivational and pharmacological effects of cocaine. Using immunohistochemistry, we observed a significant decrease in CB1 receptor expression in the prefrontal cortex, dorsal striatum, and the basolateral and basomedial amygdala following cocaine (0.5 mg/kg/infusion) self-administration. Increased CB1 receptor expression in the ventral tegmental area in rats with previous cocaine exposure was also found. Following cocaine abstinence after 10 days of extinction training, we detected increases in the expression of CB1 receptors in the substantia nigra in both cocaine groups and in the subregions of the amygdala for only the yoked cocaine controls, while any method of cocaine exposure resulted in a decrease in CB2 receptor expression in the prefrontal cortex (p < 0.01), nucleus accumbens (p < 0.01), and medial globus pallidus (p < 0.01). Our findings further support the idea that the eCB system and CB1 receptors are involved in cocaine-reinforced behaviors. Moreover, we detected a cocaine-evoked adaptation in CB2 receptors in the amygdala, prefrontal cortex, and globus pallidus.
Highlights
Cocaine is one of the most psychoactive drugs that leads to substance use disorder
Following 14 days of cocaine self-administration, the extinction training started for a separate group of animals
In the group of rats decapitated on the 10th day of extinction training, the animals pressed on the active lever more frequently than they pressed on the inactive lever from the 2nd cocaine self-administration session until the 1st day of extinction training (F(23,276) = 11.52, p < 0.001)
Summary
Cocaine is one of the most psychoactive drugs that leads to substance use disorder. The principal mechanism of action of cocaine is via monoamine Cocaine is one of the most psychoactive drugs that leads to substance use disorder. The principal mechanism of action of cocaine is via monoamine Cocaine reinforcement decreases CB1 receptor expression in the cortical and subcortical areas. 2. Cocaine abstinence results in a decrease in the expression of pallidal CB1 receptors. 3. Cocaine intake and its withdrawal change the expression of brain CB2 receptors. Apart from anandamide, the endocannabinoid system includes another endogenous ligand (2-arachidonoylglycerol), enzymes responsible for the synthesis and degradation of endocannabinoids and G protein-coupled cannabinoid receptors, namely CB1 and CB2. CB1 receptors are present in glutamatergic and GABAergic nerve endings (Kano et al 2009; Wilson and Nicoll 2002)
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