尼古丁和烟草的感官效应,Nicotine Tobacco Research

介绍

通过吸烟、吸电子烟或其他方式摄入尼古丁会引起各种影​​响，包括奖励、镇痛和因刺激、苦味和令人不快的副作用（如恶心和头晕）引起的厌恶。

目标和方法

在这里，我们回顾了尼古丁的感官效应和潜在的神经生物学过程。

结果和结论

尼古丁通过激活三叉神经伤害感受器表达的神经元烟碱乙酰胆碱受体 (nAChRs) 引起口腔刺激和疼痛。这些伤害感受器以一种被 nAChR 拮抗剂美加明显着降低的方式激发三叉神经尾核亚核 (Vc) 和其他脑干区域的神经元。Vc 神经元被尼古丁的舌部应用所激发，并且在随后的应用中表现出逐渐下降的发射，这与人类心理物理实验中外周感觉神经元的脱敏和口腔刺激等级的逐渐下降一致。尼古丁还通过刺激味觉传入引起 nAChR 介导的苦味。即使添加了甜味剂，也避免使用尼古丁溶液。采用口服自我给药的研究产生了不同的结果：一些研究表明避免尼古丁，而另一些研究则报告尼古丁摄入量随着时间的推移而增加，尤其是在青少年和女性中。据报道，尼古丁会增加人类的疼痛阈值和耐受水平。在动物研究中，尼古丁在通过吸入烟草烟雾或全身输注、鞘内注射以及通过颅内显微注射在脑桥被盖、腹外侧导水管周围灰质和延髓腹内侧延髓中传递时具有镇痛作用。抗伤害感受被认为是由脊髓伤害感受传递的下降抑制介导的。薄荷醇使尼古丁引起的口腔刺激交叉脱敏，降低刺激性，这可能是其作为烟草产品风味添加剂广受欢迎的原因。特别是在青少年和女性中。据报道，尼古丁会增加人类的疼痛阈值和耐受水平。在动物研究中，尼古丁在通过吸入烟草烟雾或全身输注、鞘内注射以及通过颅内显微注射在脑桥被盖、腹外侧导水管周围灰质和延髓腹内侧延髓中传递时具有镇痛作用。抗伤害感受被认为是由脊髓伤害感受传递的下降抑制介导的。薄荷醇使尼古丁引起的口腔刺激交叉脱敏，降低刺激性，这可能是其作为烟草产品风味添加剂广受欢迎的原因。特别是在青少年和女性中。据报道，尼古丁会增加人类的疼痛阈值和耐受水平。在动物研究中，尼古丁在通过吸入烟草烟雾或全身输注、鞘内注射以及通过颅内显微注射在脑桥被盖、腹外侧导水管周围灰质和延髓腹内侧延髓中传递时具有镇痛作用。抗伤害感受被认为是由脊髓伤害感受传递的下降抑制介导的。薄荷醇使尼古丁引起的口腔刺激交叉脱敏，降低刺激性，这可能是其作为烟草产品风味添加剂广受欢迎的原因。尼古丁通过吸入烟草烟雾或全身输注、鞘内注射以及通过颅内显微注射在桥脑被盖、腹外侧导水管周围灰质和延髓头端腹内侧进行递送时具有镇痛作用。抗伤害感受被认为是由脊髓伤害感受传递的下降抑制介导的。薄荷醇使尼古丁引起的口腔刺激交叉脱敏，降低刺激性，这可能是其作为烟草产品风味添加剂广受欢迎的原因。尼古丁通过吸入烟草烟雾或全身输注、鞘内注射以及通过颅内显微注射在桥脑被盖、腹外侧导水管周围灰质和延髓头端腹内侧进行递送时具有镇痛作用。抗伤害感受被认为是由脊髓伤害感受传递的下降抑制介导的。薄荷醇使尼古丁引起的口腔刺激交叉脱敏，降低刺激性，这可能是其作为烟草产品风味添加剂广受欢迎的原因。

影响

尼古丁会激活潜在的奖赏和镇痛作用的大脑系统，但同时会引起厌恶的感觉效应，包括口腔刺激和疼痛、苦味和其他主要由烟碱乙酰胆碱受体 (nAChR) 介导的令人不快的副作用。这篇综述讨论了尼古丁和接触烟草烟雾的相互竞争的厌恶和镇痛作用，以及潜在的神经生物学。对尼古丁相互作用的更好理解有望为减轻尼古丁和烟草使用的新方法提供信息。

"点击查看英文标题和摘要"

Sensory Effects of Nicotine and Tobacco
 

Abstract

Introduction

Ingestion of nicotine by smoking, vaping, or other means elicits various effects including reward, antinociception, and aversion due to irritation, bitter taste, and unpleasant side effects such as nausea and dizziness.

Aims and Methods

Here we review the sensory effects of nicotine and the underlying neurobiological processes.

Results and Conclusions

Nicotine elicits oral irritation and pain via the activation of neuronal nicotinic acetylcholine receptors (nAChRs) expressed by trigeminal nociceptors. These nociceptors excite neurons in the trigeminal subnucleus caudalis (Vc) and other brainstem regions in a manner that is significantly reduced by the nAChR antagonist mecamylamine. Vc neurons are excited by lingual application of nicotine and exhibit a progressive decline in firing to subsequent applications, consistent with desensitization of peripheral sensory neurons and progressively declining ratings of oral irritation in human psychophysical experiments. Nicotine also elicits a nAChR-mediated bitter taste via excitation of gustatory afferents. Nicotine solutions are avoided even when sweeteners are added. Studies employing oral self-administration have yielded mixed results: Some studies show avoidance of nicotine while others report increased nicotine intake over time, particularly in adolescents and females. Nicotine is consistently reported to increase human pain threshold and tolerance levels. In animal studies, nicotine is antinociceptive when delivered by inhalation of tobacco smoke or systemic infusion, intrathecally, and by intracranial microinjection in the pedunculopontine tegmentum, ventrolateral periaqueductal gray, and rostral ventromedial medulla. The antinociception is thought to be mediated by descending inhibition of spinal nociceptive transmission. Menthol cross-desensitizes nicotine-evoked oral irritation, reducing harshness that may account for its popularity as a flavor additive to tobacco products.电子烟烟油

Implications

Nicotine activates brain systems underlying reward and antinociception, but at the same time elicits aversive sensory effects including oral irritation and pain, bitter taste, and other unpleasant side effects mediated largely by nicotinic acetylcholine receptors (nAChRs). This review discusses the competing aversive and antinociceptive effects of nicotine and exposure to tobacco smoke, and the underlying neurobiology. An improved understanding of the interacting effects of nicotine will hopefully inform novel approaches to mitigate nicotine and tobacco use.