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R. Balster

2 papers in the library · publishing 1987-1989

Papers

Substitution and antagonism in rats trained to discriminate (+)-N-allylnormetazocine from saline.

Journal of Pharmacology and Experimental Therapeutics June 1, 1989 R. Balster

The drug (+)-N-Allylnormetazocine (NANM) binds to two sites in the mammalian brain: a high-affinity site sensitive to haloperidol and a lower-affinity site known as the phencyclidine (PCP) receptor. In rats trained to distinguish (+)-NANM from saline, drugs that bind strongly to the haloperidol-sensitive site did not produce (+)-NANM-like effects, and only haloperidol partially blocked the drug's effects, and only at doses that disrupted behavior. In contrast, PCP-like drugs from various chemical classes fully substituted for (+)-NANM, with their potency matching their affinity for the PCP receptor. The findings indicate that the PCP receptor, not the haloperidol-sensitive site, mediates the discriminative stimulus properties of (+)-NANM.

Behavioral dependence upon phencyclidine and ketamine in the rat.

Journal of Pharmacology and Experimental Therapeutics July 1, 1987 P. Beardsley, R. Balster

Continuous intravenous infusion of phencyclidine (PCP) in rats induced dependence, shown by disrupted lever-pressing behavior during withdrawal. After 10 days of PCP infusion at 0.5 mg/kg/hr, response rates dropped markedly within 6 to 12 hours and recovered within 24 to 48 hours in four rats. Re-administering PCP during withdrawal reversed the rate decline, and ketamine at 2.5 mg/kg/hr also reversed PCP withdrawal effects, indicating cross-dependence. Withdrawal from continuous ketamine infusion similarly reduced response rates in three rats, demonstrating that both drugs can produce dependence.