Quantitation of Phencyclidine in Serum by Enzyme Immunoassay: Results in 405 Patients

Walberg, Clifford B.; McCarron, Margaret M.; B, Schulze

doi:10.1093/jat/7.2.106

Cited by 35 publications

(21 citation statements)

References 4 publications

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“…Humans often repeatedly self-administer stimulants like PCP at great cost to their health (Walberg et al, 1983). Although our data suggest that the anti-PCP mAb may treat or prevent adverse effects of PCP abuse, it is unlikely to reduce craving for PCP.…”

Section: Discussionmentioning

confidence: 65%

Treatment of Adverse Effects of Excessive Phencyclidine Exposure in Rats with a Minimal Dose of Monoclonal Antibody

Laurenzana¹,

Gunnell²,

Gentry³

et al. 2003

The Journal of Pharmacology and Experimental Therapeutics

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The range of medical effects and complications resulting from excessive use of drugs of abuse like phencyclidine (PCP) has hindered the development of effective medications. Drug-specific monoclonal antibodies (mAbs) provide an appealing medication approach since they can be selective for the drug, without concern for the sites of action of the drug. The use of mAb medications has been considered impractical because it is commonly believed that very large doses of mAb would be required to treat the adverse medical effects resulting from excessive drug use. In this study, a single dose of an anti-PCP mAb was found to significantly reduce the negative health impact of excessive, prolonged PCP treatment in rats (18 mg/ kg/day for 2 weeks). The protective effects were mAb dosedependent, and mAb doses as low as 1/100th the molar equivalent amount of the PCP body burden were effective at preventing PCP-induced deaths, reducing PCP-induced behaviors, reducing PCP brain concentrations, and improving the general health status of the animals. They also show that treatment with monoclonal antibody medications can have medically important outcomes without the need to neutralize the entire dose of the offending drug. These results could help establish the feasibility of using carefully designed monoclonal antibody medications to treat drug abuse and addiction, a chronic and re-occurring illness of the central nervous system.

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Section: Discussionmentioning

confidence: 65%

Treatment of Adverse Effects of Excessive Phencyclidine Exposure in Rats with a Minimal Dose of Monoclonal Antibody

Laurenzana¹,

Gunnell²,

Gentry³

et al. 2003

The Journal of Pharmacology and Experimental Therapeutics

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“…Glycine cotreatment did not affect serum PCP levels. Serum PCP levels of the two higher doses were within the range associated with bizarre or psychosis-like behavior observed with PCP intoxication in humans (Walberg et al 1983). …”

Section: Resultsmentioning

confidence: 77%

Behavioral effects of orally administered glycine in socially housed monkeys chronically treated with phencyclidine

Linn¹,

O'Keeffe²,

Lifshitz³

et al. 2007

Psychopharmacology

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“…Although several prior studies have utilized subchronic dosing regiments, none has determined serum levels during chronic infusion. Walberg et al (1983) have demonstrated that PCP-induced psychosis is most associated with serum concentrations of up to 200 ng/ml. Serum concentrations obtained in this study were thus in the range most associated with PCP-induced psychosis, catatonia and agitation in humans.…”

Section: Pcp Blood Levelsmentioning

confidence: 99%

Subchronic Continuous Phencyclidine Administration Potentiates Amphetamine-Induced Frontal Cortex Dopamine Release

Balla

Sershen

Serra

et al. 2003

Neuropsychopharmacol

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Functional dopaminergic hyperactivity is a key feature of schizophrenia. Etiology of this dopaminergic hyperactivity, however, is unknown. We have recently demonstrated that subchronic phencyclidine (PCP) treatment in rodents induces striatal dopaminergic hyperactivity similar to that observed in schizophrenia. The present study investigates the ability of PCP to potentiate amphetamine-induced dopamine release in prefrontal cortex (PFC) and nucleus accumbens (NAc) shell. Prefrontal dopaminergic hyperactivity is postulated to underlie cognitive dysfunction in schizophrenia. In contrast, the degree of NAc involvement is unknown and recent studies have suggested that PCP-induced hyperactivity in rodents may correlate with PFC, rather than NAc, dopamine levels. Rats were treated with 5-20 mg/kg/day PCP for 3-14 days by osmotic minipump. PFC and NAc dopamine release to amphetamine challenge (1 mg/kg) was monitored by in vivo microdialysis and HPLC-EC. Doses of 10 mg/kg/day and above produced serum PCP concentrations (50-150 ng/ml) most associated with PCP psychosis in humans. PCP-treated rats showed significant, dose-dependent enhancement in amphetamine-induced dopamine release in PFC but not NAc, along with significantly enhanced locomotor activity. Enhanced response was observed following 3-day, as well as 14-day, treatment and resolved within 4 days of PCP treatment withdrawal. These findings support the concept that endogenous NMDA receptor dysfunction could account for the pattern of dopaminergic dysfunction observed in schizophrenia, and suggest that even short duration abuse of PCP-like agents may greatly potentiate behavioral effects of psychostimulants in drug abuse situations. Finally, these studies provide a model system in which to evaluate effects of potential psychotherapeutic agents.

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Quantitation of Phencyclidine in Serum by Enzyme Immunoassay: Results in 405 Patients

Cited by 35 publications

References 4 publications

Treatment of Adverse Effects of Excessive Phencyclidine Exposure in Rats with a Minimal Dose of Monoclonal Antibody

Treatment of Adverse Effects of Excessive Phencyclidine Exposure in Rats with a Minimal Dose of Monoclonal Antibody

Behavioral effects of orally administered glycine in socially housed monkeys chronically treated with phencyclidine

Subchronic Continuous Phencyclidine Administration Potentiates Amphetamine-Induced Frontal Cortex Dopamine Release

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