Institute of Physiology and Pathophysiology, Friedrich-Alexander-University Erlangen-Nürnberg, 91054 Erlangen, Germany.
Leibniz Institute for Analytical Sciences, ISAS e.V., 44227 Dortmund, Germany.
Int J Mol Sci. 2022 Feb 19;23(4):2330. doi: 10.3390/ijms23042330.
The role of TRPA1 receptor channels in meningeal nociception underlying the generation of headaches is still unclear. Activating as well as inhibitory effects of TRPA1 agonists have been reported in animal models of headache. The aim of the present study was to clarify the effect of the TRPA1 agonist nitroxyl (HNO) delivered by Angeli's salt in two rodent models of meningeal nociception. Single fibre recordings were performed using half-skull preparations of mice (C57BL/6) in vitro. Angeli's salt solution (AS, 300 µM) caused short-lasting vigorous increases in neuronal activity of primary meningeal afferents, followed by deactivation and desensitisation. These effects were similar in TRPA1 knockout and even more pronounced in TRPA1/TRPV1 double-knockout mice in comparison to wild-type mice. The activity of spinal trigeminal neurons with afferent input from the dura mater was recorded in vivo in anesthetised rats. AS (300 µM) or the TRPA1 agonist acrolein (100 and 300 µM) was applied to the exposed dura mater. AS caused no significant changes in spontaneous activity, while the mechanically evoked activity was reduced after acrolein application. These results do not confirm the assumption that activation of trigeminal TRPA1 receptor channels triggers the generation of headaches or contributes to its aggravation. Instead, there is evidence that TRPA1 activation may have an inhibitory function in the nociceptive trigeminal system.
TRPA1 受体通道在偏头痛产生的脑膜疼痛中的作用尚不清楚。在偏头痛的动物模型中,已经报道了 TRPA1 激动剂的激活和抑制作用。本研究的目的是阐明 Angeli 盐(一种含 TRPA1 激动剂亚硝酸盐(HNO)的药物)在两种脑膜疼痛啮齿动物模型中的作用。使用体外 C57BL/6 小鼠的半颅骨制备进行单纤维记录。Angeli 盐溶液(AS,300μM)引起初级脑膜传入神经纤维的短暂而剧烈的活性增加,随后失活和脱敏。在 TRPA1 敲除小鼠中,这些作用与野生型小鼠相似,而在 TRPA1/TRPV1 双敲除小鼠中更为明显。在麻醉大鼠中记录来自硬脑膜的传入输入的脊髓三叉神经神经元的活性。将 AS(300μM)或 TRPA1 激动剂丙烯醛(100 和 300μM)应用于暴露的硬脑膜。AS 对自发性活动没有显著影响,而丙烯醛应用后机械诱发的活动减少。这些结果不支持这样的假设,即三叉神经 TRPA1 受体通道的激活引发头痛的产生或加剧其恶化。相反,有证据表明 TRPA1 激活可能在伤害性三叉神经系统中具有抑制作用。