Naltrexone (0.32 mg/kg) reduces ethanol-reinforced responding at the concentration that maintained the most responding (1% or 2%) in rhesus monkeys. Naltrexone (0.1 mg/kg) reduces ethanol-reinforced responding, both at a low ethanol concentration (0.25%) that produced little ethanol intake (g/kg), and at a higher concentration (4%) with an appreciable intake. [1] Naltrexone (1-3 mg/kg) potently and dose-dependently inhibits reinstatement of ethanol-seeking produced by non-contingent deliveries of the liquid dipper filled with 8% ethanol. [2] Naltrexone elicits optimal enhancement of morphine's antinociceptive potency in mice when co-administered (i.p.) at about 100 ng/kg together with morphine (3 mg/kg). [3] Naltrexone (10 ng/kg i.p.) augments the antinociception produced by an acute submaximal dose of intrathecal (5 mg) or systemic (7.5 mg/kg i.p.) morphine in the tail-flick test in rats. Naltrexone combined with Morphine inhibits the decline in morphine antinociception and prevented the loss of morphine potency in rats. [4] Naltrexone significantly suppresses ethanol self-administration and prevents ethanol-induced increases in dialysate dopamine levels. [5] Naltrexone completely prevents the reduction in anogenital distance in prenatally stressed (PS) males and restores the growth rate of both sexes. Naltrexone also decreases the anxiety of PS rats in the plus-maze, increases the opioid component of exploration to control levels, but increases anxiety in control males. [6]