Gabriel Braley

TL;DR: It is indicated that Δ-9-THC produces a broad range of transient symptoms, behaviors, and cognitive deficits in healthy individuals that resemble some aspects of endogenous psychoses and warrant further study of whether brain cannabinoid receptor function contributes to the pathophysiology of psychotic disorders.

TL;DR: Delta-9-tetrahydrocannabinol is associated with transient exacerbation in core psychotic and cognitive deficits in schizophrenia, and this data do not provide a reason to explain why schizophrenia patients use or misuse cannabis.

TL;DR: The data suggest that frequent users of cannabis are either inherently blunted in their response to, and/or develop tolerance to the psychotomimetic, perceptual altering, amnestic, endocrine, and other effects of cannabinoids.

TL;DR: The deleterious effects of haloperidol pretreatment on the cognitive effects of Δ-9-THC are consistent with the preclinical literature in suggesting crosstalk between DAergic and CBergic systems and it is unlikely that DA D2 receptor mechanisms play a major role in mediating the psychotomimetic and perceptual altering effects.

TL;DR: These group differences may be related to the development of tolerance to the neuroendocrine effects of cannabinoids in frequent users of cannabis and not a consequence of cannabis use.