Posted by JayBTV2 on March 2, 2010, at 7:34:01
I've read in a few places (wish I had links) that some people think being on an MAOi like Parnate or Nardil would make quitting smoking easier. I guess since part of the "reward" of smoking is supposed to be MAO-B inhibition.
However doesn't the below study with Rats seem to suggest the opposite? I'm currently on Parnate and considering another attempt at quiting. Has anyone who's taken an MAOi and tried to quit find that it's helped or hurt that cause? Or even just noticed smoking more or less?
RATIONALE: The mechanisms mediating tobacco addiction remain elusive. Nicotine, the psychoactive component in tobacco, is generally believed to be the main cause of reward and addiction. However, tobacco smoke contains thousands of constituents, some of which may interact with nicotine to enhance reward. It has previously been shown that monoamine oxidase (MAO) inhibition, known to result from smoking, can enhance nicotine self-administration. The aim of the present study was to evaluate the role of noradrenergic systems in mediating this enhancement of nicotine reward. OBJECTIVE: The objective of this study was to test the hypothesis that MAO inhibitor pretreatment enhances nicotine self-administration by activation of noradrenergic pathways that regulate dopamine release in the nucleus accumbens (NAc). METHODS: The effect of prazosin (0.0625-0.5 mg/kg, i.p.), a specific alpha1-adrenergic receptor antagonist, was examined on male rats pretreated with tranylcypromine (3 mg/kg), an irreversible inhibitor of MAO A and B. Acquisition of nicotine (10 mug kg(-1) inj(-1), i.v.) self-administration behavior was examined over a 5-day period. Nicotine (60 mug kg(-1) inj(-1), i.v.)-induced increase in NAc extracellular dopamine levels was examined by in vivo microdialysis in non-self-administering animals. RESULTS: We have shown that (1) tranylcypromine enhances nicotine self-administration, (2) prazosin pretreatment blocks both the acquisition and the expression of nicotine self-administration, and (3) prazosin pretreatment diminishes nicotine-induced dopamine release in the NAc. CONCLUSION: These data indicate that the stimulation of alpha1-adrenergic receptors is critical for tranylcypromine enhancement of nicotine reward and suggest a critical interplay between the noradrenergic and dopaminergic systems in tobacco addiction.
poster:JayBTV2
thread:938344
URL: http://www.dr-bob.org/babble/20100216/msgs/938344.html