Issue Archive

Central neural mechanism of increased pain sensitivity induced by nicotine abstinence

ZHONG Jia-Hui¹, BI Yan-Zhi^2,3,*, KONG Ya-Zhuo^3,4, LU Zhi-Jie⁵, HU Li^2,3

¹Research Center of Brain and Cognitive Neuroscience, Liaoning Normal University, Dalian 116029, China；²The Key Laboratory of Mental Health, Institute of Psychology, Chinese Academy of Sciences, Beijing 100101, China；³Department of Psychology, University of Chinese Academy of Sciences, Beijing 100049, China；⁴The Key Laboratory of Behavioral Science, Institute of Psychology, Chinese Academy of Sciences, Beijing 100101, China；⁵Department of Anesthesiology, Shanghai Eastern Hepatobiliary Surgery Hospital, Shanghai 200433, China

Abstract

Nicotine is the main addictive component in cigarettes that motivates dependence on tobacco use for smokers and makes it difficult to quit through regulating a variety of neurotransmitter release and receptor activations in the brain. Even though nicotine has an analgesic effect, clinical studies demonstrated that nicotine abstinence reduces pain threshold and increases pain sensitivity in smoking individuals. The demand for opioid analgesics in nicotine abstinent patients undergoing surgery has greatly increased, which results in many side effects, such as nausea, vomiting, and respiratory depression, etc. In addition, these side effects would hinder patients’ physical and psychological recovery. Therefore, identifying the neural mechanism of the increase of pain sensitivity induced by nicotine abstinence and deriving a way to cope with the increased demand for postoperative analgesics would have enormous basic and clinical implications. In this review, we first discussed different experimental pain stimuli (e.g., cold, heat, and mechanical pain)-induced pain sensitivity changes after a period of nicotine dependence/abstinence from both animal and human studies. Then, we summarized the effects of the brain neurotransmitter release (e.g., serotonin, norepinephrine, endogenous opioids, dopamine, and γ-aminobutyric acid) and their corresponding receptor activation changes after nicotine abstinence on pain sensitivity. Finally, we discussed the limits in recent studies. We proposed that more attention should be paid to human studies, especially studies among chronic pain patients, and functional magnetic resonance imaging might be a useful tool to reveal the mechanisms of abstinence- induced pain sensitivity changes. Besides, considering the influence of duration of nicotine dependence/abstinence and gender on pain sensitivity, we proposed that the effects of nicotine abstinence and individual differences (e.g., duration of abstinence from smoking, chronic/acute abstinence, and gender) on abstinence-induced pain sensitivity should be fully considered in formulating pain treatment protocols. In summary, this paper could deepen our understanding of nicotine abstinence-induced pain sensitivity changes and its underlying neural mechanism, and could also provide effective scientific theories to guide clinical pain diagnosis and treatment, which has important clinical significance.

Key words: nicotine abstinence; pain sensitivity; neurotransmitter; receptor; mechanism

Received: 2020-12-05　　Accepted: 2021-03-12

Corresponding author: 毕研芝　　E-mail: biyz@psych.ac.cn

Citing This Article：

ZHONG Jia-Hui, BI Yan-Zhi, KONG Ya-Zhuo, LU Zhi-Jie, HU Li. Central neural mechanism of increased pain sensitivity induced by nicotine abstinence. Acta Physiol Sin 2021; 73 (6): 953-962 (in Chinese with English abstract).