الفهرس 
Acknowledgement
CORTICAL EXCITABILITYOnly 14 pages are availabe for public view
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Abstract
Nicotine is one of the main components of cigarettes and affects the central nervous system mainly via nicotinic acetylcholine receptors (nAChR). It has further effects on neuromodulation by regulating the release of: dopamine, serotonin, glutamate and adrenaline; detailed knowledge about the specific nicotinic effect on the central nervous system is still missing. In studies, it has been shown that nicotine improves attention and working memory in animals and humans, while nicotine withdrawal leads to reduced working and verbal memory capacity in otherwise healthy tobacco smokers. Since most of the cholinergic neurons terminate at presynaptic sites, acetylcholine and nicotine have been characterized primarily as neuromodulators, modulating glutamate, dopamine and GABA release. Consequently, activation of nicotine receptors can result in complex interactions involving inhibition or disinhibition of pyramidal cortical neurons. Apart from its acute effects on cortical activity and excitability, chronic nicotine exposure leads to a complex pattern of up- and down-regulation of nAChR depending on cortical region, resulting in altered brain function. Nicotine may lead to both neuronal inhibition and excitation, depending on cortical site, up- or down-regulation of receptors and mode of nicotine administration. Consequently, the net effect of the neuromodulatory action of nicotine is not easily foreseen, and the translation into functional effects is not trivial. Experiments in humans concerning acute and chronic effects of nicotine on cortical excitability are rare. In the present study, we aimed to broaden our knowledge about nicotinic impact on cortical excitability. 40 healthy cigarette smokers and 30 non-smokers, all males, participated in the study (smokers: mean age 32.8±8.9 (standard deviation) years, non-smokers: mean age 31.1±8.2 years). Subjects were recruited from Assuit university hospital outpatient clinic. All the study participants were subjected to: detailed history about onset of smoking and duration per years and number of cigarettes per day, structured clinical interview for DSM-V was used to exclude any psychiatric illness, brief neurological examination, blood sample was obtained for serum level of cotinine (active metabolite of nicotine in serum) and neurophysiological assessment. This study found that there is no difference between 1/2h after smoking and 2h after smoking in smoker group as regard motor thresholds (RMT, AMT), MEP at 130% of resting motor threshold, short latency intracortical inhibition (SICI) at ISI (1ms, 2ms, 3ms), intracortical facilitationere is significant prolongation in CSP in 2h after smoking than 1/2h after smoking and high cotinine level in 1/2h after smoking and 2h after smoking. As regard to comparison between smoker group and non-smoker group, the results show enhanced cortical inhibition, reduced facilitation, prolongation of cortical silent period in 2h after smoking in the smoker group, demonstrating a clear effect of chronic nicotine consumption on cortical excitability in humans. In summary, smoking state and acute exposure to nicotine have different effects on cortical excitability in smoking and non-smoking individuals. Whereas smokers display reduced cortical facilitation and increased inhibition as compared to non-smokers (ICF) at ISI (10ms,15ms,20ms), long latency intracortical inhibition(LICI) at ISI (50ms,100ms,150ms).However, th