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However it is notable that, unlike many other drugs of abuse, AAS do not acutely stimulate dopamine release in the nucleus accumbens (84 ). This is consistent with the relatively slow time-course of AAS action, and may account for the absence of acute intoxicating effects. Studies using the opioid antagonist naloxone have yielded variable results in AAS-treated animals. Nandrolone pretreatment enhanced withdrawal symptoms to naloxone in morphine-dependent mice (80 ), and naloxone reversed testosterone-induced locomotor depression in hamsters (75 ). However, naloxone produced virtually no effects in three rhesus monkeys exposed to two weeks of high-dose testosterone (85 ). It may be that testosterone serves as a partial opioid agonist, while also acting through several other non-opioid neurotransmitter systems. Specifically, AAS display important modulatory effects on serotonin (86 92 ), norepinephrine (89 ), dopamine (93 101 ), and gamma-amino-butyric acid (93.


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