Thomsen L L, Olesen J
Department of Neurology, Glostrup Hospital, University of Copenhagen, Denmark.
Clin Neurosci. 1998;5(1):28-33.
The molecular mechanisms of migraine pain have not yet been clarified. Neurogenic inflammation and a subsequent plasma extravasation in the dura mater have been suggested. However, monoamine and peptide neurotransmitters involved in neurogenic inflammation do not cause significant head pain. Based on our previous studies of headache induced by i.v.infusions of glyceryl trinitrate (exogenous nitric oxide donor) and histamine (which liberates nitric oxide from vascular endothelium), we suggest that nitric oxide (NO) is a more likely candidate molecule. The present review deals with the biology of this small messenger molecule and the scientific evidence suggesting a key role for this molecule in migraine headache. We hypothesise that the release of NO from either blood vessels, perivascular nerve endings, or brain tissue is a molecule trigger mechanism of spontaneous migraine pain. These novel observations dictate new approaches to the pharmacological treatment of migraine.
偏头痛疼痛的分子机制尚未阐明。有研究提出了神经源性炎症以及随后硬脑膜中的血浆外渗现象。然而，参与神经源性炎症的单胺和肽类神经递质并不会引起明显的头痛。基于我们之前对静脉输注硝酸甘油（外源性一氧化氮供体）和组胺（从血管内皮释放一氧化氮）诱发头痛的研究，我们认为一氧化氮（NO）更有可能是关键分子。本综述探讨了这种小分子信使分子的生物学特性以及表明该分子在偏头痛中起关键作用的科学证据。我们假设，从血管、血管周围神经末梢或脑组织释放的NO是自发性偏头痛疼痛的分子触发机制。这些新发现为偏头痛的药物治疗指明了新方向。
