Simons Christopher T, Sudo Satoko, Sudo Makoto, Carstens E
Section of Neurobiology, Physiology and Behavior, University of California, Davis, 1 Shields Avenue, Davis, CA 95616, USA.
Brain Res. 2003 Nov 21;991(1-2):249-53. doi: 10.1016/s0006-8993(03)03539-x.
We investigated the role of neuronal nicotinic acetylcholine receptors (nAChRs) in nicotine cross-desensitization of chemonociceptive responses of trigeminal subnucleus caudalis (Vc) neurons in rats. Vc responses to lingually applied pentanoic acid were significantly reduced following nicotine, and this was prevented when the nAChR antagonist mecamylamine was applied before or after nicotine. A peripheral site of nicotine cross-desensitization is suggested via a nAChR-mediated reduction in acidic excitation of lingual nociceptors that project to Vc.
我们研究了神经元烟碱型乙酰胆碱受体（nAChRs）在大鼠三叉神经尾侧亚核（Vc）神经元化学伤害性感受反应的尼古丁交叉脱敏中的作用。给予尼古丁后，Vc对舌部施加戊酸的反应显著降低，而在尼古丁之前或之后应用nAChR拮抗剂美加明可防止这种情况。通过nAChR介导的投射至Vc的舌部伤害感受器酸性兴奋的降低，提示了尼古丁交叉脱敏的外周部位。
