Nicotine Essay

Tobacco contains many chemicals including carcinogens like nitrosamines (210) that cause long term health complications – lung cancer, chronic obstructive pulmonary disease and heart disease being the leading causes of death (196). Nicotine, although it is not toxic relative to tobacco, it is responsible for the development of psychological dependence and withdrawal symptoms (211). It does this ultimately because chronic tobacco use causes the brain to adapt to the functional antagonism of nicotine by upregulating nicotinic receptors (202) and becoming accustomed to its positive subjective effects (209). This assignment will modify aspects from three current drugs on the market for quitting smoking to create an improved psychopharmological drug treatment. An overview of these current
Cotinine and the selective MAOB inhibitor are uncharged, lipid soluble and small, thus allowing them to pass through the blood-brain barrier (51). At the sites of action in the central nervous system, cotinine is a weak agonist for nicotine receptors (200). This causes similar effects to varenicline by making nicotine use less satisfying (214) as there is reduced activation of nicotinic receptors in the ventral tegmental area and nucleus accumbens (202). The psychological withdrawal symptoms known as nicotine abstinence syndrome is lessened because cotinine will act as a partial agonist to increase dopamine release, but not to the same magnitude as nicotine (120). Overtime, it is expected with the use of Co-MAO and gradual decrease in dosages, there should be a reduction of the number nicotinic receptors to normal levels. The selective MAOB inhibitor, helps offset the absence of other substances in tobacco that had previously inhibited monoamine oxidase activity to catabolize dopamine, norepinephrine, and serotonin