Abstract
Endogenous opioids are integral in modulating drug reward, but it is believed that these may act through several mechanisms including hypothalamic-pituitary-adrenocortical (HPA) and dopamine pathways. This study was developed to examine how nicotine dependence alters endogenous opioid regulation of prolactin response, a peripheral marker of dopaminergic activity. Smokers and nonsmokers completed two sessions during which placebo or 50 mg of naltrexone was administered, using a double-blind, counterbalanced design. Blood samples and mood measures were obtained during a resting absorption period, after exposure to two noxious stimuli (cold pressor and thermal pain), and during an extended recovery period. Opioid blockade increased prolactin response, indicating an inhibitory effect of the endogenous opioid system on prolactin, possibly mediated by reduced stimulatory effects of dopamine on this hormone. These responses were attenuated in smokers relative to nonsmokers. There was also a gender disparity in prolactin response, with women showing a stronger response to endogenous opioid modification than men regardless of smoking status. The attenuated effects of opioid blockade may reflect dysregulated opiodergic and dopaminergic effects. Results extend previous reports showing blunted opioid regulation of the HPA response in dependent smokers.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1-5 |
| Number of pages | 5 |
| Journal | Pharmacology Biochemistry and Behavior |
| Volume | 95 |
| Issue number | 1 |
| DOIs | |
| State | Published - Mar 2010 |
Bibliographical note
Funding Information:During this study Dr. al'Absi was funded by the National Institute of Health grants CA88272 and DA016351 . We thank Clemens Kirschbaum, Ph.D., of Dresden University in Germany for the help in assaying the prolactin samples and to Deanna Ellestad for the help with the data collection.
Keywords
- Dopamine
- Opioids
- Prolactin
- Reward
- Smoking
