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THE CB2-FACED RECEPTORS: IMPROVEMENT OF SLEEP OR MEMORY IN PARKINSON’S DISEASE.
Abstract
Aims
The main objective was to investigate the potential of nigrostriatal cannabinoid receptor 2 (CB2) in reverse sleep alterations observed in the animal model of Parkinson’s disease induced by rotenone. We also evaluated whether such modulation would decrease the rotenone-induced desynchronization between left and right cortical hemispheres and consequently reverse its detrimental effects on memory consolidation.
Methods
Male Wistar rats received a bilateral infusion of rotenone (12 ug/ul) or dimethylsulfoxide (DMSO, 10% v/v) within the Substantia nigra pars compacta. Seven days later, striatal infusions of CB2 agonist GW405833 (10 ug/ul), antagonist AM630 (3 ug/ul), or vehicle (DMSO 10% v/v) were performed. One set of animals was submitted to a period of 6h of sleep-wake recording and the other to a memory evaluation.
Results
CB2 antagonist AM630 reversed the rotenone effects on sleep macrostructure, establishing the values of sleep efficiency and NREM sleep duration to that observed in the control group. In the same way, the rotenone-induced desynchronization between left and right cortical hemispheres was reversed by CB2 blockade. However, AM630 did not present an effect on memory consolidation. Instead, the activation of CB2 by GW405833 was able to reverse the memory impairment induced by rotenone.
Conclusions
These findings suggest a role for nigrostriatal CB2 in sleep regulation in the context of Parkinson’s disease. Its effect on memory consolidation appears to be independent of sleep and cortical synchronization.