Nicotine Addiction Research Paper

Addiction is a troubling problem that is prevalent in every part of the world. Many people do not understand addictions. The common misconception is that people who are addicted have trouble with quitting because they lack the determination or do not have any self-control. However, this is not always the case. Addiction, especially when pertaining to drug abuse, is a disease that affects the brain in ways that lends itself to compulsive actions. The two questions that can be drawn from this misconception are: “How does one get addicted to drugs in the first place?” and “Why does this develop into the inability to exit the addiction?” This paper will explore the cellular mechanisms that pertain to these two questions on addiction. The

According to I. P. Stolerman and M. J. Jarvis’s research, “evidence clearly identifies nicotine as a powerful drug of addiction, comparable to heroin, cocaine and alcohol.” (Stolerman 2). Exploring the pathway of nicotine addiction is a good way to understand, in detail, the cellular mechanisms of addiction. Nicotine starts by binding to nAChRs. nAChRs are receptors that belong to a superfamily of ligand-gated ion channels. The receptor-channel complex is composed of five polypeptide subunits assembled like a rosette around a central water-filled pore. There are many different subunit combinations, but only one, alpha seven is spread throughout the mammalian central nervous system. The main endogenous agonist, naturally produced receptor binding partner, for all nAChRs is acetylcholine, but nicotine is also an agonist (Dani 440). Acetylcholine are important neuro transmitters that apply to every drug of abuse addiction mechanism. Substances that interfere with acetylcholine binding are called anticholinergics (Costa 2). At a synapse in the central nervous system, acetylcholine is transported by the presynaptic terminal at a concentration of about 1 mM for a couple of milliseconds before the acetylcholine is hydrolyzed by acetylcholinesterase. Nicotine acquired from tobacco arrives much more slowly, at a concentration of only .1 microM, and it is present much longer because nicotine cannot be broken down by acetylcholinesterase. The longer presence and lesser concentration of agonist favors desensitization (Dani 440). This meaning that now Nicotinic receptors can exist on the cell’s surface as nonfunctional receptors, making it harder for acetylcholine to bind to nAChRs than before. This all happens before entering the central nervous system. The important thing to take form this being that Acetylcholine tries to bind to nAChRs in order to reach the Central Nervous System as a