Table 4.
Cocaine Use Disorders | |||
---|---|---|---|
References | Type of Sample | Type of Evaluation | Outcomes |
[462] | Human | Post-mortem | ↓ CB1r and GRK2/3/5 in the PFC in CoUDs |
[463] | Animals | CB1r KO vs WT mice | 25% of the CB1r KO mice compared to the 75% of their WT littermates acquired a reliable operant responding to self-administration of cocaine, and the number of sessions required to attain this behavior was ↑ in CB1r KO mice. |
[464] | Animals | Glu-CB1r vs GABA-CB1r KO vs WT | CB1r expression in forebrain GABAergic neurons-controlled sensitivity to cocaine, while CB1r expression in cortical glutamatergic neurons controlled the associative learning processes. |
[465] | Animals | D1-CNR1 KO vs A2a-CNR1 KO vs WT mice |
D1-CNR1 KO mice did not display hyperlocomotion in response to acute cocaine dosing. D1-CNR1 and A2a-CNR1 KO mice exhibited blunted locomotor activity across repeated cocaine doses A2a-CNR1 KO mice did not express a preference for cocaine paired environments in a two-choice place preference task. |
[466] | Animals | Male Long Evans rats | Systemic cocaine increased premature responding, a measure of impulsivity. |
[467] | Animals | Transgenic mice overexpressing the CB2r vs WT littermates | Overexpression of the CB2r significantly ↓ motor response to acute administration of cocaine cocaine-induced motor sensitization, CPP, and cocaine self-administration. |
[427] | Animals | DAT-CNR2 KO vs WT mice | DAT-CNR2 KO mice enhanced psychostimulant-induced hyperactivity but an absence of psychostimulant-induced sensitization compared to WT mice. |
[468] | Animals | Male Wistar rats | Following cocaine self-administration, a ↑ CB1r expression in the VTA and a ↓ CB1r expression in the PFC, dorsal striatum, and AMY. Cocaine abstinence, ↑CB1r expression in the SN and the AMY, and a ↓ CB2r expression in the PFC, NAcc, and medial globus pallidus. |