Simmons Steven J, Gould Thomas J
Department of Psychology, Neuroscience Program, Temple University, Philadelphia, PA, 19122, USA.
J Clin Pharm Ther. 2014 Oct;39(5):457-67. doi: 10.1111/jcpt.12171. Epub 2014 May 14.
Tobacco smoking remains a major health problem. Nicotine binds to nicotinic acetylcholine receptors (nAChRs), which can cause addiction and withdrawal symptoms upon cessation of nicotine administration. Pharmacotherapies for nicotine addiction target brain alterations that underlie withdrawal symptoms. This review will delineate the involvement of the β2 subunit of neuronal nAChRs in nicotine reward and in generating withdrawal symptoms to better understand the efficacy of smoking cessation pharmacotherapies.
Chronic nicotine desensitizes and upregulates β2 subunit-containing nAChRs, and the prolonged upregulation of receptors may underlie symptoms of withdrawal. Experimental research has demonstrated that the β2 subunit of neuronal nAChRs is necessary for generating nicotine reward and withdrawal symptoms.
Smoking cessation pharmacotherapies act on β2 subunit-containing nAChRs to reduce nicotine reward and withdrawal symptom severity.
吸烟仍然是一个主要的健康问题。尼古丁与烟碱型乙酰胆碱受体（nAChRs）结合，在停止给予尼古丁后会导致成瘾和戒断症状。尼古丁成瘾的药物疗法针对构成戒断症状基础的大脑改变。本综述将阐述神经元nAChRs的β2亚基在尼古丁奖赏及产生戒断症状中的作用，以更好地理解戒烟药物疗法的疗效。
慢性尼古丁会使含β2亚基的nAChRs脱敏并上调，而受体的长期上调可能是戒断症状的基础。实验研究表明，神经元nAChRs的β2亚基对于产生尼古丁奖赏和戒断症状是必需的。
戒烟药物疗法作用于含β2亚基的nAChRs，以降低尼古丁奖赏及戒断症状的严重程度。
