Chronic phencyclidine administration induces schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in rat brain.
Lindsay M Reynolds, Susan M Cochran, Brian J Morris, Judith A Pratt, Gavin P Reynolds
Schizophrenia research March 1, 2005 DOI: 10.1016/j.schres.2004.02.003 via PubMed
Summary
AI-generated from the abstractRepeated 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.
Study at a glance
| Characteristics | Observational study Peer reviewed |
|---|---|
| Population | Rats |
| Intervention | Phencyclidine (PCP) |
| Duration | Chronic intermittent regime |
| Key finding | Chronic intermittent PCP administration in rats produced NAA and NAAG deficits only in the temporal cortex and elevated NAAG in the hippocampus, closely reflecting postmortem findings in schizophrenia. |
Abstract
Administration of phencyclidine (PCP) to both humans and animals models the symptoms of schizophrenia. Brain concentrations of N-acetylaspartate (NAA) are reduced in this disease, reflecting neuronal dysfunction. This study investigates the effects in rats of a chronic intermittent regime of PCP on NAA and its precursor N-acetylaspartylglutamate (NAAG) in rat frontal and temporal cortex, hippocampus and striatum, determined by HPLC. We found significant PCP-induced deficits of NAA and NAAG only in the temporal cortex; NAAG was significantly elevated in the hippocampus. These changes closely reflect postmortem findings reported in schizophrenia.