PCP (Phencyclidine): An Update

Abstract

The steady rise in the promiscuous use of phencyclidine (PCP) as a "recreational" drug has recently gained nationwide attention because of the numerous violent and/or bizarre incidents caused by the use of this drug. Because the media often exaggerate reports of bizarre and violent behavior to make a "good" story, the potential PCP user may be tempted to ignore the media warnings. In the case of PCP, however exaggerated the story, a real danger does exist. So, despite numerous newspaper, radio and television warnings about the possible consequences of PCP use and abuse, the incidence of toxic reactions continues to climb. In many cases PCP is sold as other drugs, particularly THC, and in various colored capsules, tablets, liquids and crystals which may explain the increased usage despite the numerous warnings against its use. The advances in laboratory techniques and chemical processess have enabled the clandestine chemist to prepare relatively pure PCP and thus eliminate many of the toxic side effects due to impurities in the drug. In addition, 30 or more psychoactive PCP analogues have been developed and are starting to make an appearance on the street. PCP is perhaps the most potent psychotomimetic compound known at the present time and is capable of inducing a psychosis which is clinically indistinguishable from schizophrenia. The psychosis-producing effects of PCP are the most common toxic effects seen in hospital emergency rooms; but as the amount of PCP taken and/or the simultaneous involvement of other drugs, particularly barbiturates, occurs, severe medical problems (e.g., coma, seizures, respiratory arrest) begin to appear. Death from high doses of PCP or PCP plus other drugs does occur, but the principal cause of death from PCP abuse is due to trauma, homicide or suicide (usually of the bizarre or violent form). Young adult males, persons predisposed to mental illness and naive drug users appear to be the most susceptible to the adverse effects of PCP. The fact that chronic PCP users are starting to increase in number is mute testimony that not all users experience "bad trips" with PCP. Unfortunately for the user, however, this does not guarantee that the next trip will not be a bad one. The effects of chronic use seem to be twofold: severe depression with suicidal thoughts and numerous violent, agitated behavioral patterns. Neither seems to be a suitable alternative. At the present time there is not specific antidote for toxic PCP reactions and the prolonged psychosis induced in some cases does not appear to respond to the standard antipsychotic medications as quickly as do the functional psychoses. The major improvement from a medical standpoint is the development of more sensitive laboratory techniques to confirm the presence of PCP in body fluids. This advance has undoubtedly led to the apparent increase in the number of PCP cases reported by hospitals and to the accuracy of clinical diagnosis by medical, drug or law enforcement communities...

Cell-based therapies for the treatment of schizophrenia

“…The first group to test this hypothesis used the phencyclidine (PCP) model of schizophrenia. PCP, an NMDA antagonist induces acute psychosis in humans 95 and can produce schizophrenia-like deficits in rodents 22,23 . Using the sub-acute PCP model, Tanaka and colleagues demonstrated that deficits in novel object recognition and prepulse inhibition were prevented by transplanting MGE tissue into the medial prefrontal cortex (mPFC) of newborn animals 96 .…”

Effect of PDE10A inhibitors on MK-801-induced immobility in the forced swim test

“…In their seminal review, Jentsch and Roth (1999) describe that the positive symptoms dominate after acute intake of PCP/ketamine, whereas after chronic intake, negative symptoms become more obvious. Garey (1979) outlined that the effects of chronic PCP use seem to be twofold: severe depression with suicidal thoughts and numerous violent, agitated behavioural patterns. De Angelis and Goldstein (1978) also describe anxiety as an additional symptom.…”

Interactions of the mGluR5 gene with breeding and maternal factors on startle and prepulse inhibition in mice

“…Early support for the glutamate hypothesis of schizophrenia came from suggestions that non-competitive antagonists of the NMDA receptor [such as phencyclidine (PCP), dizocilpine (or MK-801), and ketamine] partially mimic both positive and negative symptoms of schizophrenia when administered to healthy humans (Luby et al, 1959;1962;Allen and Young, 1978;Garey, 1979;Snyder, 1988;Javitt and Zukin, 1991). While there are reports of the NMDA antagonist ketamine disrupting PPI in healthy humans (Karper et al, 1995), there have also been reports of ketamine administration resulting in a slight increase in PPI (Duncan et al, 2001;Abel et al, 2003).…”