Gibbs J L, Hargreaves K M
Department of Endodontics, University of Texas Health Science Center in San Antonio, TX, USA.
J Dent Res. 2008 Oct;87(10):948-52. doi: 10.1177/154405910808701008.
Neuropeptide Y (NPY) is an important modulatory neuropeptide that regulates several physiological systems, including the activity of sensory neurons. We evaluated whether activation of the NPY Y1 receptor could modulate the activity of capsaicin-sensitive nociceptors in trigeminal ganglia and dental pulp. We tested this hypothesis by measuring capsaicin-stimulated calcitonin gene-related peptide release (CGRP) as a measure of nociceptor activity. Capsaicin-evoked CGRP release was inhibited by 50% (p < 0.05) in trigeminal ganglia and by 26% (p < 0.05) in dental pulp when tissues were pre-treated with [Leu(31),Pro(34)]NPY. The Y1 receptor was found to co-localize with the capsaicin receptor TRPV1 in trigeminal ganglia. These results demonstrate that activation of the Y1 receptor results in the inhibition of the activity of capsaicin-sensitive nociceptors in the trigeminal ganglia and dental pulp. These findings are relevant to the physiological modulation of dental nociceptors by endogenous NPY and demonstrate an important novel analgesic target for the treatment of dental pain.
神经肽Y(NPY)是一种重要的调节性神经肽,可调节包括感觉神经元活动在内的多种生理系统。我们评估了NPY Y1受体的激活是否能调节三叉神经节和牙髓中对辣椒素敏感的伤害感受器的活动。我们通过测量辣椒素刺激的降钙素基因相关肽释放(CGRP)作为伤害感受器活动的指标来验证这一假设。当用[亮氨酸(31),脯氨酸(34)]NPY预处理组织时,三叉神经节中辣椒素诱发的CGRP释放被抑制了50%(p<0.05),牙髓中被抑制了26%(p<0.05)。发现Y1受体与三叉神经节中的辣椒素受体TRPV1共定位。这些结果表明,Y1受体的激活导致三叉神经节和牙髓中对辣椒素敏感的伤害感受器的活动受到抑制。这些发现与内源性NPY对牙齿伤害感受器的生理调节有关,并证明了治疗牙齿疼痛的一个重要的新镇痛靶点。