Abstract
Since the identification and cloning of the cannabinoid receptor 2 (CB2R), several studies focused on the characterization of its physiological and pathological role. Initially, CB2R was considered as the peripheral cannabinoid receptor due to its detection in the rat spleen and leukocyte subpopulation in humans. Later, CB2R was identified in different brain regions significantly modifying the landscape and pointing out its role in a wide variety of central physiological functions and pathological conditions. Additional research also detected the expression of CB2R in neurons, microglia, and astroglia in different brain regions. Indeed, the findings collected to date support a significant function of CB2R in anxiety, depression, schizophrenia, and additional neuropsychiatric disorders. This review gathers the most relevant literature regarding new advances about the role of CB2R in a variety of neuropsychiatric conditions, with special emphasis on its potential as a new therapeutic target for the treatment of different psychiatric disorders.
Highlights
The cannabinoid receptor 2 (CB2R) along with the cannabinoid receptor 1 (CB1R) are the receptors of the endogenous cannabinoid system (ECS)
Research focused on elucidating the physiological role and therapeutic utility of cannabinoid receptor 1 CB2R (CB1R) in neuropsychiatry since it was the first cannabinoid receptor identified in the central nervous system (CNS)
This review summarizes the main findings highlighting the involvement of CB2R in different physiological processes such as stress response, emotional reactivity, and cognitive processing that are affected in different psychiatric disorders
Summary
The cannabinoid receptor 2 (CB2R) along with the cannabinoid receptor 1 (CB1R) are the receptors of the endogenous cannabinoid system (ECS). The results found with the conditional knockout mouse lacking CB2R in dopaminergic neurons (DAT-Cnr2-/-) are similar, that is, they present increased immobility time in the tail suspension and forced swimming tests, suggesting increased vulnerability to stimuli promoting depressive-like behaviors in rodents [51] (Table 2).
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