Biological Constricts of Cigarette Smoking

Widely recognized as a an addictive habit, similar to alcoholism and drug abuse, “Tobacco addiction is best considered a chronic disease, with most smokers requiring repeated interventions over time before achieving permanent abstinence.” Even with these multiple interventions, it is to the non-smoker’s wonder as to why there is no cessation in habit, even when fully knowing all health effects. Studies have shown that out of the 80% of smokers who give forth attempts to quit relapse within a month, and only a mere 3% make it to six months of a smoke-free outlook.

 With nicotine causing pleasurable effects that induce a habit, this pleasure soon turns over for its dire health consequences like heart diseases, cancer, and emphysema. Repeated exposure increases receptors and induces a increased tolerance and thus a dependence to reach that high. These changes in brain function are what induce such strong appetitive needs for cigarettes. 

Though many will never understand the inner-battle that smoker’s take on in quitting, Daniel S. McGehee study of nicotine and the biological role it plays on the body published an article titled “Nicotine Potentiation of Excitatory Inputs to Ventral Tegmental Area Dopamine Neurons.” He had visited Loyola University Chicago on February 24^th, speaking upon his topic of research to a Neuroscience Seminar class. Through his study it was found that nicotine worked to activate receptors that brought forth changes in the ventral tegmental area of the brain. In the nicotinic receptors that are activated, it was found that a strong preference in   synaptic strength towards appetitive behaviors and addictions were induced.

Nicotine was seen to induce long-term potentiation (LTP) in the VTA (DA) neurons by increasing glutamate release on glutamate terminals, suggesting the importance of the presynaptic strength that induced through the effects of nicotine. In many experiments that were taken up in his paper, presynaptic modulation of excitatory transmission in excitatory synaptic current found increased levels of both nicotine and SKF 81297. Adding to the effects of nicotine, this part of experimentation went to further show that there is a pair-pulse stimulation to bring forth data that showed in vivo exposure of nicotine to brain slices from drug-naïve rats induced excitatory synaptic plasticity. When compared to much more widely known addictive drugs like cocaine, there was much overlap within the biological circuitry amongst the two physical substance use effects.

Article Source: http://www.nytimes.com/2008/05/20/health/20brod.html

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