NICOTINE AFFECTS ON TEENAGERS

Nicotine Affects on Teenagers

Nicotine Affects on Teenagers

Introduction

Nicotine is one of the most-used psychoactive drugs in the world. The primary psychoactive active ingredient in tobacco is nicotine. According to the 2005 National Survey on Drug Use and Health (Department of Health and Human Services, 2006), about 71.5 million Americans (> 12 years old) used a tobacco product within the previous month. Only 30.6 percent of full-time college students ages 18 to 22 reported using in the previous month, as compared to 42.7 percent of same-aged part-time and non-college students. Many of the toxic chemical compounds, other than nicotine, in tobacco products are the source of serious health problems (e.g., emphysema, chronic lung disease, cancer, cardiovascular disease) and death. (Levin, McClernon and Rezvani 2006, 523-539)

Nicotine is easily absorbed into the body. When inhaled, nicotine in cigarette smoke particles (tar) is quickly absorbed into the bloodstream via the capillaries lining the lungs. Smokers experience a sudden “rush” with that first cigarette of the day because the nicotine-saturated blood rapidly reaches the brain and crosses the BBB. Even though cigarettes contain about 0.5 to 2.0 mg of nicotine, smokers absorb only about 20 percent of that nicotine into blood. Smokers easily avoid nicotine toxicity by controlling the depth and rate of smoke inhalation. The liver metabolizes about 90 percent of the nicotine in the bloodstream before excretion. Urine tests measuring nicotine's major metabolite cotinine do not distinguish between tobacco use and environmental exposure. (Levin and Simon 1998, 217-230)

Nicotine is an agonist at acetylcholinergic nicotinic receptors. Peripherally, nicotine's activation of receptors increases blood pressure, heart rate, and adrenal gland release of adrenaline. Nicotine activation of CNS nicotinic receptors located on presynaptic terminal buttons facilitates release of dopamine, acetylcholine, and glutamate throughout the brain. Physiological and psychological dependence of nicotine is due to nicotinic-induced release of dopamine from neurons projecting from the ventral tegmental area to forebrain regions (mesolimbic system) and prefrontal cortex (mesocortical system), brain areas responsible for reinforcement. Nicotine-induced release of acetylcholine is the likely cause of improved cognition and memory, as well as increased arousal. Increased glutamatergic activity due to nicotinic presynaptic facilitation contributes to enhanced memory of nicotine users.

Plenty of evidence exists regarding nicotine's facilitating effects on cognition and memory in humans and animals (for reviews see Levin, McClernon, & Rezvani, 2006; Levin & Simon, 1998). Individual differences in the cognitive effects of nicotine may be due to genetic variations in dopaminergic activity. Nicotine administered via a patch to adult carriers of the 957T allele (alters D2 receptor binding in humans) impaired working verbal memory performance and reduced processing efficiency in brain regions important for phonological rehearsal. Additionally, nicotine stimulates activity in brain regions involved in attention, motivation, mood, motor activity, and arousal.

Tolerance appears to develop to the subjective mood effects of nicotine, but not to nicotine-induced changes in physiology or behavioral performance. However, most smokers do develop both physiological and psychological dependence on nicotine. Typically, withdrawal from cigarettes causes intense persistent cravings, irritability, apprehension, irritation, agitation, fidgeting, trouble concentrating, ...