Nicotine and the Brain: Articles and Studies
In one report in Archives of Environmental Health, Dr. Brautbur discusses the direct effects nicotine causes on the brain that would prove that nicotine is addictive. Brautbur's presentation of data from the 1980's would force one to agree that nicotine is addictive; specific activities on the nervous system, with specific receptors; and that both animals and human develop addiction. Within this article, experts, such as the U.S. Surgeon General, report that smokers experience three classic signs of addiction: 1) they become dependent; 2) they want to quit but cannot; 3) they become tolerant, although a plateau is reached. Smokers, however, must take large doses to reach that plateau (1).
In this article, Brautbur reports that nicotine causes arousal while building up a tolerance. As one smokes more cigarettes, one accumulates more and more nicotine in the body; resulting in a greater level of tolerance. Simply, as a person smokes more and more, the brain develops a certain level at which nicotine is required so that the brain can continue receiving pleasure. Because this level becomes increasing large as more nicotine is introduced, it becomes more difficult to satisfy the brain. Thus, many smokers experience withdrawal symptoms (1).
Further, Brautbur discusses past studies which examined the effects of nicotine on animals. Brautbur reports that nicotine activates certain neurons in part of the brain called the mesolimbic system. This system is the same pathway that creates the intense cravings to indulge in certain foods or activities, such as sex. When the mesolimbic pathway is stimulated, the neurons secrete dopamine. In turn, dopamine provides the brain with a chemical reward that literally arouses it. Tests have shown that both cocaine and nicotine produce this effect in the brain. In general, nicotine continually stimulates the release of dopamine (1).
To support this claim, another article by Dr. Benowitz in the Annual Review of Pharmacology and Toxicology reports the results of self-administered nicotine in animals. Animals, such as rats or monkeys, self-administered nicotine at dose levels comparable to those taken in by human smokers. Studies in rats have shown that nicotine effects the mesolimbic system. Nicotine, like that of cocaine, causes the mesolimbic system to project from the ventral tegmental area of the midbrain to the nucleus accumbens. Nicotine increases the firing of ventral tegmental area neurons that, in turn, releases neurotransmitters in this system (2).
Both articles reported that nicotine has been shown to increase cerebral glucose metabolism. Dr. Brautbur reports that when rats developed a heightened brain metabolic activity after they received increased doses of nicotine. This heightened brain activity was an increase in cerebral glucose uptake. According to Dr. Brautbur, changes in brain energy utilization have been observed in association with drugs, such as cocaine (1). In Dr. Benowitz's article, regions with increased cerebral glucose metabolism also had high-affinity nicotine binding (2).
In an experiment performed in England, the effects of nicotine were related to that of amphetamines and cocaine. Both amphetamines and cocaine release dopamine in the nucleus accumbens and increase locomotor activity. According to this report, recent studies have shown that nicotine induces the release of dopamine in the nucleus accumbens. This present study only confirmed that a systematic injection of nicotine can increase extracellular levels of dopamine in the nucleus accumbens of rats. Not only that, nicotine also increased locomotor activity and head-bobbing behavior (3).