N-acetylaspartylglutamate levels in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue. It also induces symptoms in humans that mimic schizophrenia. PCP not only produced symptoms similar to schizophrenia, it also yielded electroencephalogram changes in the thalamocortical pathway (increased delta decreased alpha) and in the hippocampus (increase theta bursts) that were similar to those in schizophrenia. PCP-induced augmentation of dopamine release may link the NMDA and dopamine hypotheses of schizophrenia. Pharmacokinetics PCP is metabolized into PCHP, PPC and PCAA. The drug is metabolized 90% by oxidative hydroxylation in the liver during the first pass. Metabolites are glucuronidated and excreted in the urine. Nine percent of ingested PCP is excreted in its unchanged form. When smoked, some of the compound is broken down by heat into 1-phenylcyclohexene (PC) and piperidine. The time taken before the effects of PCP manifest is dependent on the route of administration. The onset of action for inhalation occurs in 2–5 minutes, whereas the effects may take 15 to 60 minutes when ingested orally. Chemistry PCP is an arylcyclohexylamine. Analogues Fewer than 30 different analogs of PCP were reported as being used on the street during the 1970s and 1980s, mainly in the United States. Only of a few of these compounds were widely used including rolicyclidine (PCPy), eticyclidine (PCE), and tenocyclidine (TCP). Less common analogs include 3-HO-PCP, 3-MeO-PCMo, and 3-MeO-PCP. The generalized structural motif required for PCP-like activity is derived from structure-activity relationship studies of PCP derivatives. All of these derivatives are likely to share some of their psychoactive effects with PCP itself, although a range of potencies and varying mixtures of anesthetic, dissociative, and stimulant effects are known, depending on the particular drug and its substituents. In some countries such as the United States, Australia, and New Zealand, all of these compounds would be considered controlled substance analogs of PCP under the Federal Analog Act and are hence illegal drugs if sold for human consumption. History PCP was initially made in 1956 and brought to market as an anesthetic medication. Its use in humans was disallowed in the United States in 1965 due to the high rates of side effects, while its use in animals was disallowed in 1978. Moreover, ketamine was discovered and was better tolerated as an anesthetic. PCP is classified as a schedule II drug in the United States. A number of derivatives of