Cannabinoid drugs affect sensorimotor gating deficits in spontaneously hypertensive rats (SHRs), a strain used as an animal model of schizophrenia. SHRs showed reduced prepulse inhibition (PPI) compared to Wistar rats, indicating impaired sensorimotor gating. The cannabinoid agonist WIN55212 (1 mg/kg) and cannabidiol (30 mg/kg) reversed this PPI deficit, while the CB1 antagonist rimonabant (0.75 mg/kg) worsened it. The anandamide uptake inhibitor AM404 had no effect. These findings suggest cannabinoid drugs may offer therapeutic strategies for schizophrenia-related sensorimotor gating impairments.
Harmine, a component of the psychedelic brew ayahuasca, impairs memory in emotional contexts in rats, and even untreated rats housed with harmine-treated rats show memory deficits. In experiments using contextual and tone fear conditioning and a plus-maze discriminative avoidance task, harmine at 10 mg/kg impaired contextual fear conditioning, and all doses (5, 10, or 15 mg/kg) impaired discriminative avoidance. Untreated rats housed in cages with harmine-treated rats also showed memory deficits across all tasks, suggesting that social context and cohabitation can influence the drug's behavioral effects.