Rats given phencyclidine (PCP) for 7 days showed increased DNA methylation at one of two specific sites in the parvalbumin gene promoter in both the prefrontal cortex and hippocampus six weeks later, compared to rats given a vehicle. No change was seen in a global measure of DNA methylation. This hypermethylation may contribute to parvalbumin neuron deficits in this animal model of psychosis, which are also observed in schizophrenia.
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.