Posted by Larry Hoover on June 10, 2003, at 6:51:46
In reply to Re: Nicotine and brain chemicals, posted by samplemethod on June 10, 2003, at 6:30:52
> I would be interested in finding scientific evidence that nicotine is a MAO-B inhibitor. My impression was the cigarettes, or more correctly something within the cigarettes when smoked, actually affects MAO-B. It may well be nicotine, but I havent seen any proof of that yet.
>
>
> CheersQuite right. I did a sloppy reading of the originally posted abstract, and had a similar incorrect statement. Nicotine isn't an MAOI, but cigarette smoke is (probably from cotinine). It comes as no surprise then, why nicotine replacement is an incomplete substitute for smoking.
Nicotine Tob Res. 2001 Nov;3(4):383-90.
Platelet monoamine oxidase, smoking cessation, and tobacco withdrawal symptoms.
Rose JE, Behm FM, Ramsey C, Ritchie JC Jr.
VA Medical Center, and Department of Psychiatry, Duke University Medical Center, Durham, North Carolina 27705, USA. [email protected]
Previous studies have found that constituents in tobacco inhibit both forms of the enzyme monoamine oxidase (MAO-A and MAO-B). This enzyme is important in the breakdown of the amine neurotransmitters, including dopamine, which is thought to mediate the reinforcing effects of nicotine and contribute to tobacco dependence. To further examine the relationship between cigarette smoking, smoking cessation and MAO, we measured platelet MAO-B activity in 16 smokers before and after being switched to smoking denicotinized cigarettes; in a subset of six subjects who subsequently quit-smoking, MAO-B activity was also measured at 1 and 4 weeks following cessation. Smoking cessation treatment was provided in an open-label format, and included nicotine skin patch treatment in conjunction with oral mecamylamine (a nicotinic antagonist) and neostigmine (a peripherally acting acetylcholinesterase inhibitor, administered to counteract constipation experienced from mecamylamine). Results showed that smoking behavior, indexed by expired air carbon monoxide levels, was negatively correlated with platelet MAO-B activity prior to smoking cessation. Moreover, MAO-B activity significantly increased by approximately 100% at 4 weeks after quitting smoking. However, little or no recovery occurred within the first week of abstinence, suggesting that the constituents in tobacco responsible for MAO inhibition may have half-lives of several days. Thus, if relapse to smoking is due in part to withdrawal from the MAO-inhibiting effects of tobacco, this effect likely occurs more than 1 week after quitting. Additionally, low baseline MAO-B activity significantly predicted the intensity of withdrawal symptoms reported upon switching to the denicotinized cigarettes as well as after smoking cessation. These results support the view that MAO inhibition from non-nicotine constituents in cigarette smoke is relevant to tobacco dependence and that continued investigation of the potential use of MAO inhibitors in smoking cessation treatment is warranted.
Int J Neuropsychopharmacol. 2001 Mar;4(1):33-42.
Monoamine oxidases and tobacco smoking.
Berlin I, Anthenelli RM.
Department of Pharmacology, Pitie-Salpetriere University Hospital, Paris, France. [email protected]
Although nicotine has been identified as the main ingredient in tobacco responsible for aspects of the tobacco dependence syndrome, not all of the psychopharmacological effects of smoking can be explained by nicotine alone. Accumulating preclinical and clinical evidence has demonstrated that smoking also leads to potent inhibition of both types (A and B) of monoamine oxidase (MAO). Smokers have 30-40 % lower MAOB and 20-30 % lower MAOA activity than non-smokers. Reduced MAO activity in smokers has been shown by direct measures (platelets, positron emission tomographic studies) or by indirect measures (concentration of monoamine catabolites in plasma or CSF). We examine the hypothesis that chronic habitual smoking can be better understood in the context of two pharmacological factors: nicotine and reduced MAO activity. We speculate that MAO inhibition by compounds found in either tobacco or tobacco smoke can potentiate nicotine's effects. Based on this concept, more effective anti-smoking drug strategies may be developed. As a practical consequence of tobacco smoke's MAO-inhibitory properties, comparative psychiatric research studies need to screen and control for tobacco use.
poster:Larry Hoover
thread:232715
URL: http://www.dr-bob.org/babble/20030609/msgs/232838.html