title: [Neuropeptide effects on the trigeminal system: pathophysiology and clinical significance for migraine].
abstract: Neuropeptides, such as calcitonin gene-related peptide (CGRP), substance P and vasoactive intestinal polypeptide (VIP) are considered important mediators in primary headaches. Increased concentrations of CGRP have been found in jugular venous plasma during attacks of migraine and, concomitant with VIP elevation, during cluster headache. Substance P and CGRP are produced from subsets of trigeminal afferents whereas VIP derives from parasympathetic efferents. Release of these neuropeptides in the meninges causes arterial vasodilatation, mast cell degranulation and plasma extravasation in animal experiments. Particularly CGRP seems to be important, as receptor antagonists have recently been shown to have a therapeutic effect on migraine. Animal models have confirmed the role of CGRP in meningeal nociception. The activity of spinal trigeminal neurons is a sensitive integrative measure of trigeminal activity and CGRP released from central terminals of trigeminal afferents in the spinal trigeminal nucleus has been shown to facilitate nociceptive transmission, most likely by a presynaptic action. The proposed CGRP functions are supported by the distribution of CGRP receptor components localized in the rat cranial dura mater, the trigeminal ganglion and the spinal trigeminal nucleus. The currently available data indicate multiple sites of CGRP action in trigeminal nociception and the pathogenesis of migraine but central CGRP receptors are probably the essential targets in the treatment of migraine using CGRP receptor antagonists.
authors.affiliation: Institut für Physiologie und Pathophysiologie, Universität Erlangen-Nürnberg, Erlangen, Deutschland Messlinger@physiologie1.uni-erlangen.de
authors.forename: K
authors.initials: K
authors.lastname: Messlinger
authors.forename: M J M
authors.initials: MJ
authors.lastname: Fischer
authors.forename: J K
authors.initials: JK
authors.lastname: Lennerz
mesh_terms: D000344:Afferent Pathways / Q000503:physiopathology; D000818:Animals; D015740:Calcitonin Gene-Related Peptide / Q000502:physiology*; D003027:Cluster Headache / Q000503:physiopathology; D004195:Disease Models, Animal; D006801:Humans; D008881:Migraine Disorders / Q000503:physiopathology*; D009619:Nociceptors / Q000502:physiology; D051381:Rats; D018015:Receptors, Calcitonin Gene-Related Peptide / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D013373:Substance P / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology; D012668:Trigeminal Ganglion / Q000503:physiopathology; D014276:Trigeminal Nerve / Q000503:physiopathology*; D014279:Trigeminal Nucleus, Spinal / Q000503:physiopathology; D014660:Vasoactive Intestinal Peptide / Q000502:physiology*
chemical_list: D018015:Receptors, Calcitonin Gene-Related Peptide; D013373:Substance P; D014660:Vasoactive Intestinal Peptide; D015740:Calcitonin Gene-Related Peptide