Neuroscience: Nicotine and Brain

The paper discusses the topic of nicotine influence on brain. The specific mechanisms of nicotine dependence and their effects on various brain receptors are discussed. The paper refers to the mechanisms of nicotine and alcohol interaction and their relation to neurological processes in the human brain. The paper evaluates the impacts which nicotine produces on impulsive behaviors in humans and its effects on attention and other cognitive processes.

The role of new pharmacological treatments of nicotine addiction is discussed. The paper suggests several directions for the future research. Neuroscience: Nicotine and Brain Nicotine dependence and smoking addiction present one of the most serious health problems in present day world. Million of smokers die every year of health complications related to smoking. Thousands of social and advertising campaigns are being developed to reduce the scope of the issue and to teach individuals the dangers of smoking.

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That smoking addiction is associated with the complex brain mechanisms and reactions is difficult to deny: a wealth of literature was written to describe the specific processes that occur in animal and human brain under the influence of nicotine. Nicotine dependence is one of the most interesting topics in neuroscience. Better knowledge of nicotine-responsive receptors and the knowledge of nicotine-related mechanisms in the human brain must, finally, let medical professionals and scholars develop a sound pharmacological strategy, aimed to reduce nicotine dependence and facilitate withdrawal from nicotine among tobacco addicts.

In light of the current knowledge about nicotine and its relation to brain, researchers must concentrate on investigating possible genetic predispositions to chronic smoking and develop pharmacological solutions necessary to help individuals cope with their dependence on nicotine. Nicotine and Brain: The Nature of Addiction Much was written and said about how nicotine affects human brain. Thousands of experiments were performed to better understand the mechanisms of nicotine interaction with brain and the mechanisms behind smoking addiction and cessation in humans.

Today, researchers generally agree that nicotinic acetylcholine receptors, Ach-glutamate mechanisms, and chronic nicotine-induced adaptations are among the major brain mechanisms responsible for the development and maintenance of nicotine addiction in animals and humans (Zheng, Spiller & Gardiner, 2009). Nicotine “is an alkaloid that binds to central and peripheral nicotinic acetylcholine receptors” (Zheng, Spiller & Gardiner, 2009).

In its turn, acetylcholine is a neurotransmitter that activates and binds to nAChRs (Zheng, Spiller & Gardiner, 2009). The latter are the ion channels formed from the combination of five subunits that are abundant in the brain and tend to be localized on somatodendrites or postsynaptic cells (Zheng, Spiller & Gardiner, 2009). The activation of these postsynaptic cells in brain results in increased excitability and, consequentially, increases the influx of Ca++ via brain neurotransmitters and channels (Zheng, Spiller & Gardiner, 2009).

These mechanisms, however, present only a part of the complex interaction between nicotine and brain: Ach-glutamate mechanisms play a fundamental role in mediating the rewarding effects of nicotine on brain receptors and neurotransmitters and reinforce psychostimulant effects of addictive drugs (Zheng, Spiller & Gardiner, 2009). The current state of research does not provide compelling evidence to the thesis that Ach-glutamate mechanisms are solely responsible for the development and maintenance of nicotine addiction in humans (Zheng, Spiller & Gardiner, 2009).

The lack of knowledge about other areas of human brain implies that the real mechanisms of the nicotine-brain interaction can be much more sophisticated (Zheng, Spiller & Gardiner, 2009). This is, probably, one of the basic reasons why postmodern science regularly fails to develop a sound system of smoking addiction treatment for humans. The majority of smokers confess that the first cigarette they smoke during the day produces the most significant effects on their organism.

These reports imply that regular exposure to nicotine leads to the development of desensitization; the latter is, actually, the reflection of the desensitization that occurs in ? 4? 2 nAChRs receptors on the brain cell surface (Zheng, Spiller & Gardiner, 2009). Simultaneously, the repeated use of nicotine is the direct prerequisite for the development of locomotor sensitization, which is also mediated by ? 4? 2 subunits (Zheng, Spiller & Gardiner, 2009).

All these neuroadaptations can be responsible for the development of nicotine addiction, although the specific mechanism of these sensitizations is yet to be discovered. More often than not, the mechanisms of nicotine-brain interaction are associated with the release of dopamine (Gardner et al. 2009). Nicotine in blood activates dopamine neurons and pathways, which cause dopamine release to the nucleus accumbens (Gardner et al. , 2009).

The latter is responsible for the onset of nicotine dependence in animals and humans (Gardner et al. 2009). The knowledge of dopamine release mechanisms suggests that nicotine dependence is not as simple as researchers believe it to be. Moreover, nicotine dependence is hardly a social habit but is a complex neurobiological process. During the periods of withdrawal, individuals tend to experience a number of symptoms, from restlessness and irritability to insomnia and even physical pain (Gardner et al. , 2009).

These are the signs of the homeostatic misbalance in various brain systems, which follow the absence of regular dopamine releases and result of the lack of rewarding brain experiences that naturally accompany the use of nicotine. For many years, researchers believed that one cannot develop nicotine dependence, until having smoked several years in a row; many others were confident that withdrawal symptoms were a peculiar feature in those, who smoked more than five cigarettes a day because of the high levels of nicotine in their blood (Gardner et al. , 2009).

Yet, novice smokers experience withdrawal symptoms even if they smoke a few cigarettes per week (Gardner et al. 2009). Gardner et al. (2009) write that occasional smoking suppresses their withdrawal symptoms, but the duration of relief from smoking a single cigarette gradually reduces due to the development of sensitization – the effects which were also discussed by Zheng, Spiller and Gardiner (2009). To keep withdrawal in check, a novice smoker will need to smoke more and more cigarettes and at more frequent intervals, eventually reaching the point where 10-20 cigarettes a day is a norm.

The interval between finishing one cigarette and smoking another one is usually called “latency of withdrawal”, and can last from several minutes to several days and even weeks (Gardner et al. , 2009). Today, researchers face the need to understand, what mechanisms and neurotransmitters are responsible for latency (e. g. , serotonin and beta-endorphin). Nicotine and Alcohol: The Interactions With the Human Brain Many smokers notice that the combination of nicotine and alcohol produces specific effects on their cognition and brain.

Moreover, many non-regular smokers confess having an increased desire to smoke a cigarette under the influence of alcohol. Actually, nicotine-alcohol interactions present one of the most interesting and controversial topics in neuroscience. Recent findings regarding the ways in which alcohol and nicotine influence the human brain vary. Nevertheless, it is possible to assume that alcohol and nicotine produce complex effects on the human brain through a number of mechanisms and neurotransmitters.

For example, chronic nicotine administration is responsible for the decrease of norepinephrine release in the hippocampus and the decrease of basal extracellular levels of dopamine in the nucleus assumbens (Lajtha & Sershen, 2010). Both alcohol and nicotine equally affect the changes in endocannabinoid contents of the human brain (Lajtha & Sersen, 2010). Ultimately, alcohol induces the decrease of nicotine-dependent dopamine while nicotine, in its turn, is responsible for the decrease in alcohol-induced dopamine release (Lajtha & Sersen, 2010).

These changes have a marked impact on the individual desire to smoke a cigarette and to drink alcohol, to compensate for these dopamine decreases and changes. Not all alcohol- and nicotine-related changes in human brain are additive – some of them would be mutually exclusive. For example, Jamal et al. (2010) suggest that nicotine and alcohol alone influence significantly the cholinergic markers in brain, while their combined use does not produce any effects on these markers. These interactions, according to Jamal et al. (2010), could contribute to the frequent combined use of alcohol and nicotine by smokers.

They would seek more rewarding experiences under the influence of the two different substances. However, even without alcohol, nicotine reflects in impulsivity and affects human cognitive processes, including attention and task completion. The knowledge of these brain mechanisms is extremely useful for the development of sound pharmacological solutions to nicotine dependence. Nicotine: Impulsive Behaviors and Cognitive Processes The link between nicotine and impulsive behaviors has long been the subject of the professional research.

That nicotine influences human behaviors and reactions is no longer a secret, but the exact mechanisms of these interactions and effects remain unknown. Tsutsui-Kimura et al. (2010) suggest that impulsive behaviors and premature reactions under nicotine are the expressions of the inhibitory control that attenuates the connectivity of the infralimbic cortex with the motor cortex in brain. Another suggestion is that impulsive behaviors follow the modulation of the neural activities of the nucleus accumbens through the activation of the already mentioned here ? 4?

2 receptors (Tsutsui-Kimura et al. , 2010). These impulsive behaviors may have different consequences: they may reflect in the heightened risks of smoking initiation or disrupt smoking cessation (Tsutsui-Kimura et al. , 2010). Better understanding of these processes will help to develop strategies necessary for individuals to escape the vicious circle of nicotine dependence on tobacco use. Impulsive behaviors are not the only effects of nicotine influence on brain. Nicotine influences a variety of cognitive processes, including attention, thinking, and task completion.

Surprisingly or not, smoking and nicotine lead to the activation of areas that are normally associated with selective attention (Rose et al. 2010). Under the influence of nicotine, individuals display better attention and improved task completion skills (Rose et al. , 2010). The fact is that attention is not necessarily driven by a dedicated neural control but grows from the activation of various parietofrontal circuits (Rose et al. , 2010). However, where regular smokers display better accuracy, their reaction time for input and output information processing is longer compared with non-smokers (Rose et al., 2010).

Today, researchers must concentrate on the analysis of mechanisms and functional changes that lead to the facilitation of accuracy among smokers and non-smokers. The knowledge of neuromechanisms and the effects of nicotine on human brain are essential for the development of effective pharmacological approaches to tobacco dependence. For example, Brody et al. (2009) confirm that inhalation of nicotine during smoking is solely responsible for the occupancy of brain receptors that participate in the development of nicotine addiction. Brody et al.

(2009) prove that smoking denicotinized cigarettes leads to similar occupancy: as a result, denicotinized cigarettes can substantially alleviate withdrawal symptoms. That means that substances and compounds other than nicotine may be responsible for the development of nicotine dependence. A few current neuropharmacological solutions have proved to be relatively effective for treating nicotine addiction. These are bupropion and varenicline – the preparations that interfere with nicotine’s actions “in the mesolimbic DA reward and relapse system” (Zheng, Spiller & Gardiner, 2009).

Unfortunately, the current knowledge of nicotine induced mechanisms in the human brain is incomplete. Future research must concentrate on (a) the development of nicotine addiction medications that would normalize the function of nicotinic receptors; and (b) the analysis of genetic factors responsible for the development of resistance to nicotine replacement therapies and neuropharmacological solutions to nicotine dependence (Berrettini, 2008). Today, there is still much to do, in order to have full understanding of the interactions between nicotine and brain.

Conclusion That nicotine produces multiple effects on human brain is a well-known fact. The interactions between nicotine and brain present one of the most challenging topics in neuroscience: as more and more people are becoming dependent on smoking, professionals in medicine seek to understand the specific mechanisms of nicotine addiction, to be able to develop effective pharmacological solutions to the problem. Today, the effects of nicotine on the human brain are associated with the dopamine release and the activation of nicotinic acetylcholine receptors.

Nicotine is believed to generate impulsive behaviors. The combination of nicotine and alcohol and its influence on brain is another frequent subject of professional analysis. Future research must concentrate on the analysis of potential genetic factors that lead to the development of pharmacological resistance to nicotine replacement therapies, and develop medications that would normalize the function of nicotinic receptors in human brain. References Berrettini, W. (2008). Nicotine addiction.

The American Journal of Psychiatry, 165, 9, 1085- 1092. Brody, A. L. , Mandelkern, M. A. , Costello, M. R. , Abrams, A. L. & Scheibal, D. (2009). Brain nicotinic acetylcholine receptor occupancy: Effect of smoking a denicotinized cigarette. International Journal of Neuropsychopharmacology, 12, 305-316. Gardner, P. D. , Tapper, A. R. , King, J. A. , DiFranza, J. R. (2009). The neurobiology of nicotine addiction: Clinical and public policy implications. The Journal of Drug Issues, 39, 2, 417-441. Jamal, M. , Ameno, K., Miki, T. , Tanaka, N. , Ohkubo, E. & Kinoshita, H. (2010).

Effects of systemic nicotine, alcohol or their combination on cholinergic markers in the frontal cortex and hippocampus of rat. Neurochemistry Research, 35, 1064-1070. Lajtha, A. & Sershen, H. (2010). Nicotine: Alcohol reward interactions. Neurochemistry Research, 35, 1248-1258. Rose, E. J. , Ross, T. J. , Kurup, P. K. & Stein, E. A. (2010). Nicotine modulation of information processing is not limited to input (attention) but extends to output (intention).

Psychopharmacology, 209, 291-302. Tsutsui-Kimura, I. , Ohmura, Y. , Izumi, T. , Yamaguchi, T. , Yoshida, T. & Yoshioka, M. (2010). Nicotine provokes impulsive-like action by stimulating ? 4? 2 nicotinic acetylcholine receptors in the infralimbic, but not in the prelimbic cortex. Psychopharmacology, 209, 35`-359. Zheng, X. I. , Spiller, K. & Gardner, E. L. (2009). Mechanism-based medication development for the treatment of nicotine dependence. Acta Pharmacol Sin, 30, 6, 723-739.


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