Repeated intermittent doses of phencyclidine (PCP) in rats caused deficits of N-acetylaspartate (NAA) and its precursor N-acetylaspartylglutamate (NAAG) specifically in the temporal cortex, while NAAG was elevated in the hippocampus. These changes mirror postmortem findings in schizophrenia, supporting the use of PCP-treated rats as a model for the neuronal dysfunction seen in that disease.
Psychotic patients who tested positive for cannabis and those who did not were indistinguishable in their psychopathology, diagnoses, illness onset, and demographic backgrounds. The only difference was in substance use history. This suggests that psychosis occurring alongside cannabis use does not have a distinctive presentation or onset pattern and is not limited to any specific ethnic or socioeconomic group, offering little support for 'cannabis psychosis' as a separate diagnostic category.