Table 1.
Author/year | HIV animal model and subject characteristics | Cannabinoid measure/manipulation | Cognitive assessments | Cognitive domains | Main findings |
---|---|---|---|---|---|
Jacobs et al. 2019 | Mouse—iTat (50% female) 7/group: Tat + /Tat − |
Measured CB1R expression | Go/no-go task | Inhibitory-control | Female iTat + mice demonstrated less inhibitory-control compared to male iTat + mice and had higher CB1R expression in mPFC relative to all other groups; Higher infralimbic mPFC CB1R expression correlated with less inhibitory-control |
League et al. 2021 | Mouse—iTat (100% female) | MAG-L inhibition via MJN110 | Discrimination and reversal-learning task | Learning and cognitive flexibility | Initial and reversal-learning was quicker in Tat + mice than in Tat − mice; MJN 110 slowed reversal-learning to Tat- levels |
12/group: Tat +/Tat− | |||||
Wang et al. 2022 | Rat-hippocampal gpl20 injection (100% male) 8–9/group: control, sham, gpl20 |
eCB agonist WIN-55,212–2 (3 mg/kg) and/or CB2R antagonist AM630 (1.5 mg/kg) prior to gpl20 | Morris water maze | Learning and memory | Prophylactic WIN-55,212–2 treatment attenuated Gpl20-induced spatial memory deficits; WIN-55,212–2 effects were blocked by CB2R antagonist treatment, which also prevented hippocampal gpl20-induced inflammation and apoptosis |
Winsauer et al. 2011 | Rhesus monkeys (100% males) | Acute THC (0.032–0.32 mg/kg; IM); | Repeated acquisition task | Learning/working memory | Prior to SIV acute THC decreased response-rates without affecting %errors; tolerance developed to chronic THC irrespective of SIV. Chronic THC did not affect viral load but reduced neuropathology, opportunistic infections and inflammation in SIV + animals, and decreased hippocampal CB1R and CB2R expression across all animals (SIV + / −) |
3–4/group: SIV + / − ; THC + / − | Chronic 28-day THC (2×/day; 0.32 mg/kg; IM) |