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首页> 美国卫生研究院文献>Scientific Reports >Compromised neuroplasticity in cigarette smokers under nicotine withdrawal is restituted by the nicotinic α4β2-receptor partial agonist varenicline
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Compromised neuroplasticity in cigarette smokers under nicotine withdrawal is restituted by the nicotinic α4β2-receptor partial agonist varenicline

机译：烟碱α4β2-受体部分激动剂缬草胺能恢复尼古丁戒断后吸烟者的神经可塑性受损

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Nicotine modulates neuroplasticity and improves cognitive functions in animals and humans. In the brain of smoking individuals, calcium-dependent plasticity induced by non-invasive brain stimulation methods such as transcranial direct current stimulation (tDCS) and paired associative stimulation (PAS) is impaired by nicotine withdrawal, but partially re-established after nicotine re-administration. In order to investigate the underlying mechanism further, we tested the impact of the α4β2-nicotinic receptor partial agonist varenicline on focal and non-focal plasticity in smokers during nicotine withdrawal, induced by PAS and tDCS, respectively. We administered low (0.3 mg) and high (1.0 mg) single doses of varenicline or placebo medication before stimulation over the left motor cortex of 20 healthy smokers under nicotine withdrawal. Motor cortex excitability was monitored by single-pulse transcranial magnetic stimulation-induced motor evoked potential amplitudes for 36 hours after plasticity induction. Stimulation-induced plasticity was absent under placebo medication, whereas it was present in all conditions under high dose. Low dose restituted only tDCS-induced non-focal plasticity, producing no significant impact on focal plasticity. High dose varenicline also prolonged inhibitory plasticity. These results are comparable to the impact of nicotine on withdrawal-related impaired plasticity in smokers and suggest that α4β2 nicotinic receptors are relevantly involved in plasticity deficits and restitution in smokers.
机译：尼古丁调节动物和人类的神经可塑性并改善其认知功能。在吸烟者的大脑中，尼古丁戒断会损害非侵入性脑刺激方法（如经颅直流电刺激（tDCS）和配对联想刺激（PAS））诱导的钙依赖性可塑性，但在尼古丁重用后部分恢复管理。为了进一步研究其潜在机制，我们测试了分别由PAS和tDCS诱导的烟碱戒断期间α4β2-烟碱样受体局部激动剂伐尼克兰对吸烟者局灶性和非局灶性可塑性的影响。在尼古丁戒断对20名健康吸烟者的左运动皮层进行刺激之前，我们先给予了低剂量（0.3μmg）和高剂量（1.0μmg）的伐尼克兰或安慰剂药物。运动性皮层兴奋性由可塑性诱导后单脉冲经颅磁刺激诱导的运动诱发电位振幅监测36小时。安慰剂治疗下没有刺激引起的可塑性，而高剂量下在所有情况下都存在。低剂量仅恢复了tDCS诱导的非局灶可塑性，对局灶可塑性没有明显影响。高剂量伐尼克兰还可以延长抑制可塑性。这些结果可与烟碱对吸烟者戒断相关的可塑性损害的影响相当，并表明α4β2烟碱样受体与吸烟者的可塑性缺乏和恢复有关。

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