Behavioural Neuroscience Poster Session

Re: Poster 668

Peter M. Liebmann

On Fri Dec 4, grover wrote
>Dr. Liebmann: Great poster.  Hope you are having fun at the meeting. "Data from animal experiments reveal some effects of nicotine to be mediated through endogenous opioids, suggesting a common neurophysiological pathway of nicotine- and heroin dependence."  Opiate receptors are involved in at least a hundred different regulatory pathways in the body.  It is not clear if you are suggesting that there are data in the literature which show that in animals smoking and/or nicotine potentiate heroine addiction.  Perhaps, another way to look at these data is purely from a sociological view-point rather than a metabolic one.  Any comments?

Dr. Grover: thank you for your comment. It has been found that nicotine releases endogenous opioids in rats (Davenport et al. 1990. Neurosci-Lett. 113: 40-46). In humans the opioid antagonist naloxone reduces the attractiveness of smoking (Gorelicket al. 1988. J. Subst. Abuse, 1: 153-159). From these data it was reasonable to hypothesize that endogenous opioids participate in the nicotine induced reinforcing mechanism for smoking (Aceto et al. 1993. Eur. J. Pharmacol. 248: 333-335).
In your last sentence you address a key question in the discussion on substance dependence: It is certainly right that social factors have a great impact on the development and maintenance of substance dependence in general. This is well documented and completely out of doubt. However, in addition to that there is accumulating evidence of genetic (metabolic) factors predisposing to substance dependence (alcoholism is best investigated and there this fact is well established already). The fact that substance dependence has also a metabolic component and thus has to be qualified as an organic disease has social and socioeconomic consequences. A better understanding of the pathophysiological basis may open up new ways of therapy, which are urgently needed looking at the enormous relapse rate.

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