Oxytocin has been shown to modulate the development of acute and chronic tolerance to multiple drugs of abuse, including the analgesic effect of morphine and heroin (Kovacs et al., 1984, Kovacs et al., 1987), physiological effects of alcohol (i.e., sedative, ataxia, and hypothermic effects) (Szabo et al., 1987, Szabo et al., 1985, Szabo et al., 1989, Jodogne et al., 1991, Puciklowski et al., 1985, Tirelli et al., 1992), and sensitization to hyperactivity and stereotyped behavior associated with psychostimulants (Sarnyai et al., 1992). Early preclinical work demonstrated that both peripheral and central OXT dose-dependently attenuated the development of analgesic opioid tolerance and a single OXT injection (1 mg/kg) blocked the expression of established chronic opiate tolerance (Kovacs et al., 1985, Kovacs et al., 1984, Kovacs et al., 1987). Additionally, OXT pre-treatment inhibited the development of tolerance to morphine-induced hyper-locomotion (Kovacs et al., 1987) and anti-nociceptive effects (Kovacs et al., 1985) in mice. With regards to psychostimulants, higher doses of OXT have been shown to reduce locomotor hyperactivity and stereotyped behaviors induced by cocaine (Kovacs et al., 1990, Sarnyai et al., 1991,
