Major findings supporting the involvement of CB2R in depressive disorders
|Genetic studies||Genetic manipulation||Animal specie||Experimental test||Behavioral changes||References|
|CB2xP||Mouse, ICR||TST||↓ immobility time|||
|NSFT||↓ latency time and ↑ food (g) consumption|||
|CMS||↑ resistance(↑ sucrose 1% consumption and ↓ immobility time in TST)|||
|CB2–/–||Mouse, ICR||TST||↑ immobility time|||
|DAT-Cnr2–/–||Mouse, C57BL/6J||TST, FST||↑ immobility time|||
|Pharmacological studies||Drug||Animal specie||Experimental test||Dosis||Behavioral changes||References|
|AM630 (CB2R antagonist)||Mouse, ICR||CMS||1 mg/kg per 12 h (4 weeks)||Antidepressive actions (↑ immobility time in TST and ↑ sucrose 1% consumption)|||
|Mouse, BALB/c C57BL/6J||CMS||3 mg/kg per 24 h (4 weeks)||No effect|||
|Q63R polymorphism||Japanese||↑ incidence|||
|CB2R expression||Caucasian||↓ in DLPFC and amygdala|||
TST: tail suspension test; NSFT: novelty suppressed feeding test; FST: forced swimming test; CMS: chronic mild stress
We thank all participants in this study. We greatly appreciated Biorender for helping to create figure 1.
MSGG and JM conceived the presented idea. MSGG took the lead in writing the manuscript. FN and AG wrote the manuscript in consultation with MSGG. All authors provided critical feedback and helped shape the research, analysis, and manuscript.
The authors declare no conflict of interest.
© The Author(s) 2021.