PRL secretion from the anterior pituitary is primarily inhibited by dopamine. Acute cigarette smoke significantly increased PRL secretion and the increase in PRL levels correlated with increased plasma nicotine levels [6]. When subjects smoked nicotine-free cigarettes, PRL levels were unchanged [6]. Significant increases in PRL levels in response to opioid blockade have also been observed [7]. However, the response is significantly diminished in smokers, relative to nonsmokers [7]. Because dopamine inhibits PRL secretion, opioids increase dopamine secretion that results in an inhibition of PRL secretion. Therefore, these data suggest that smokers may have blunted opioid-mediated dopamine release or dysregulated interactions between dopamine and PRL [7]. Considering the importance of dopamine levels in nicotine addiction, dysregulation of dopamine-release may play a role in the mechanism of addiction associated with nicotine. In light of the stimulatory effects of nicotine on dopamine levels one would expect a decrease in PRL secretion, given the inverse relation between dopamine and PRL. Decreased PRL levels are observed in long-term, but not acute smoking, possibly due to desensitization of the nAChRs [8].