Ebersberger A, Takac H, Richter F, Schaible H-G
Department of Physiology, Friedrich-Schiller-University of Jena, Jena, Germany.
Cephalalgia. 2006 Mar;26(3):282-9. doi: 10.1111/j.1468-2982.2005.01035.x.
Although not without controversy, an influence of the autonomic nervous system in headache is a matter for current debate. A possible contact site of autonomic and sensory nerves is the dura mater, where they form a dense network accompanying blood vessels. We investigated interactions between autonomic and nociceptive fibres by measuring release of calcitonin gene-related peptide (CGRP) and prostaglandin E2 (PGE2) from the dura mater, in vitro. The parasympathomimetic agent carbachol did not change basal release of CGRP or PGE2, whereas it diminished release induced by a mixture of inflammatory mediators. Norepinephrine did not change induced release of CGRP or PGE2, nor basal release of CGRP. However, basal release of PGE2 was enhanced by norepinephrine, and this enhancement was reduced by serotonin through 5-HT(1D) receptors. We conclude that sympathetic transmitters may control nociceptor sensitivity via increased basal PGE2 levels, a possible mechanism to facilitate headache generation. Parasympathetic transmitters may reduce enhanced nociceptor activity.
尽管存在争议，但自主神经系统在头痛中的作用仍是当前的一个讨论话题。自主神经与感觉神经的一个可能接触部位是硬脑膜，它们在那里形成一个伴随血管的密集网络。我们通过体外测量硬脑膜中降钙素基因相关肽（CGRP）和前列腺素E2（PGE2）的释放，研究了自主神经纤维与伤害性感受纤维之间的相互作用。拟副交感神经药卡巴胆碱并未改变CGRP或PGE2的基础释放量，然而它却减少了由炎症介质混合物诱导的释放。去甲肾上腺素并未改变诱导的CGRP或PGE2释放量，也未改变CGRP的基础释放量。但是，去甲肾上腺素增强了PGE2的基础释放量，而5-羟色胺通过5-HT(1D)受体降低了这种增强作用。我们得出结论，交感神经递质可能通过提高基础PGE2水平来控制伤害感受器的敏感性，这可能是促进头痛发生的一种机制。副交感神经递质可能会降低增强的伤害感受器活性。
