Skip to content

Jibran Y. Khokhar

3 papers in the library · 7 citations · publishing 2024-2026

Papers

Randomized Laboratory Study of Single-Dose Cannabis, Dronabinol, and Placebo in Patients With Schizophrenia and Cannabis Use Disorder

Schizophrenia Bulletin June 20, 2024 Mary F. Brunette, Robert M. Roth, Christi L. Trask et al. 5 citations

A single modest dose of oral THC (15 mg dronabinol) worsened verbal learning and attention in people with schizophrenia and co-occurring cannabis use disorder, without exacerbating psychotic symptoms several hours after administration. Smoked low-dose THC cigarettes did not produce these cognitive effects. Higher blood THC levels were linked to increased negative symptoms. Drug liking was greater with THC than placebo. The findings suggest that oral THC may impair cognition in this population even at modest doses, while not acutely worsening psychosis.

Tetrahydrocannabivarin (THCV) Dose Dependently Blocks or Substitutes for Tetrahydrocannabinol (THC) in a Drug Discrimination Task in Rats

Biomolecules September 18, 2025 Hakan Kayır, Larissa Kouroukis, Iman Aziz et al. 2 citations

Delta-9-Tetrahydrocannabivarin (THCV), a natural cannabinoid similar to THC, can both mimic and block some of THC's effects depending on dose. In a study with 16 male rats trained to distinguish THC from a placebo, THCV partially substituted for THC at 3 mg/kg (54.6% of responses), but at 6 mg/kg it reversed the effects of a low THC dose. THCV did not alter blood levels of THC or its metabolite 11-OH-THC. The results suggest THCV acts as a partial CB1 receptor agonist, producing a mix of agonist and antagonist effects.

Which Came First? Utility of Preclinical Models in Cracking the Chicken-or-Egg Relationship between Cannabis Use and Schizophrenia

Current Addiction Reports February 27, 2026 Amanda C. Lee, Jibran Y. Khokhar

Cannabis use is linked to schizophrenia, especially in vulnerable people. Preclinical rodent models help clarify this relationship by allowing controlled experiments that are impossible in humans. Recent studies use advanced paradigms, including translationally-relevant rodent models and ecologically valid cannabis administration routes, to simulate human use patterns and vulnerability. These models show that cannabinoid exposure can alter schizophrenia-like behaviors and neural effects related to hyperlocomotion, sensorimotor gating deficits, social withdrawal, and anhedonia. The route of administration, dose, and type of cannabinoid shape these outcomes. Such findings identify periods of heightened vulnerability and inform prevention and intervention strategies.