Phencyclidine (PCP) can cause acute and lasting psychoses in humans and is used in animal models of psychosis. In rats, acute PCP disrupts prepulse inhibition (PPI) of the startle reflex, similar to deficits seen in schizophrenia. It was unclear whether sustained PCP exposure also disrupts PPI. This study gave rats PCP for 5 days via osmotic minipumps or for 14 days via repeated injections. PPI was disrupted only during drug administration, not after it stopped. PPI does not appear sensitive to the neuropathological effects of sustained PCP exposure.
Phencyclidine (PCP) can cause a psychosis resembling schizophrenia and dementia that sometimes persists long after the drug is stopped. In rats, a five-day continuous 'binge' of PCP caused lasting increases in brain glucose metabolism, especially in limbic regions (retrosplenial, piriform, and entorhinal cortex, hippocampus, and olfactory tubercle). These increases were still present 10 days after the drug was removed, indicating that the metabolic changes persist. The findings suggest a brain basis for the prolonged psychosis that can follow PCP use.