Mediatorwirkungen im trigeminovaskulären system als grundlage für die nozizeptiven vorgänge bei der kopfschmerzentstehung

Translated title of the contribution: Actions of nociceptive mediators in the trigeminovascular system as a basis for the generation of headaches

Karl Meßlinger, R. De Col, T. Denekas, M. Dux, M. Eberhardt, S. V. Koulchitsky, J. Röder, P. M. Schlechtweg, M. L. Sixt, N. Schwenger, T. Strecker, M. Tröltzsch, M. J M Fischer

Research output: Contribution to journalArticle

Abstract

Nociceptive mechanisms in the trigeminovascular system are probably involved in the generation of different forms of hedaches, wherein the neuropeptide CGRP (calcitonin gene-related peptide), which is released from a subset of activated primary afferents, is regarded as an important mediator. CGRP is not only a potent vasodilator but is also involved in nociceptive transmission in the trigeminal nucleus. Inhibition of CGRP receptors by the high-affinity CGRP receptor antagonist BIBN4096BS, which had proved its therapeutic potency in migraine patients, led to a significant decrease in neuronal activity in the spinal trigeminal nucleus of the rat. Another important vasodilatory mediator in meningeal nociception seems to be nitric oxide (NO), which may facilitate CGRP release from peripheral and central trigeminal structures. Inhibition of NO generation was effective in lowering the neuronal activity in the spinal trigeminal nucleus as well, whereas infusion of NO donors led to an increase in activity. The activiation showed typically a biphasic pattern. The delayed response can only be explained by secondary processes such as the expression of pro-nociceptive substances in the trigeminal nucleus or ganglion, as indicated by preliminary experimental studies. The fact that clinical and basic experimental data complement each other highlights the interpretative value of basic experiments for the pathophysiological mechanisms underlying the generation of headaches.

Original languageGerman
Pages (from-to)504-507
Number of pages4
JournalAktuelle Neurologie
Volume34
Issue number9
DOIs
Publication statusPublished - Nov 2007

Fingerprint

Calcitonin Gene-Related Peptide
Spinal Trigeminal Nucleus
Calcitonin Gene-Related Peptide Receptors
Trigeminal Nuclei
Headache
Nitric Oxide
Trigeminal Ganglion
Nociception
Nitric Oxide Donors
Neuropeptides
Migraine Disorders
Vasodilator Agents
Inhibition (Psychology)
Therapeutics

Keywords

  • BIBN4096BS
  • CGRP
  • Headache
  • Nitric oxide
  • Trigeminovascular system

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Meßlinger, K., De Col, R., Denekas, T., Dux, M., Eberhardt, M., Koulchitsky, S. V., ... Fischer, M. J. M. (2007). Mediatorwirkungen im trigeminovaskulären system als grundlage für die nozizeptiven vorgänge bei der kopfschmerzentstehung. Aktuelle Neurologie, 34(9), 504-507. https://doi.org/10.1055/s-2007-970952

Mediatorwirkungen im trigeminovaskulären system als grundlage für die nozizeptiven vorgänge bei der kopfschmerzentstehung. / Meßlinger, Karl; De Col, R.; Denekas, T.; Dux, M.; Eberhardt, M.; Koulchitsky, S. V.; Röder, J.; Schlechtweg, P. M.; Sixt, M. L.; Schwenger, N.; Strecker, T.; Tröltzsch, M.; Fischer, M. J M.

In: Aktuelle Neurologie, Vol. 34, No. 9, 11.2007, p. 504-507.

Research output: Contribution to journalArticle

Meßlinger, K, De Col, R, Denekas, T, Dux, M, Eberhardt, M, Koulchitsky, SV, Röder, J, Schlechtweg, PM, Sixt, ML, Schwenger, N, Strecker, T, Tröltzsch, M & Fischer, MJM 2007, 'Mediatorwirkungen im trigeminovaskulären system als grundlage für die nozizeptiven vorgänge bei der kopfschmerzentstehung', Aktuelle Neurologie, vol. 34, no. 9, pp. 504-507. https://doi.org/10.1055/s-2007-970952
Meßlinger, Karl ; De Col, R. ; Denekas, T. ; Dux, M. ; Eberhardt, M. ; Koulchitsky, S. V. ; Röder, J. ; Schlechtweg, P. M. ; Sixt, M. L. ; Schwenger, N. ; Strecker, T. ; Tröltzsch, M. ; Fischer, M. J M. / Mediatorwirkungen im trigeminovaskulären system als grundlage für die nozizeptiven vorgänge bei der kopfschmerzentstehung. In: Aktuelle Neurologie. 2007 ; Vol. 34, No. 9. pp. 504-507.
@article{693afb71b25c448eb1fc7656d3dd510a,
title = "Mediatorwirkungen im trigeminovaskul{\"a}ren system als grundlage f{\"u}r die nozizeptiven vorg{\"a}nge bei der kopfschmerzentstehung",
abstract = "Nociceptive mechanisms in the trigeminovascular system are probably involved in the generation of different forms of hedaches, wherein the neuropeptide CGRP (calcitonin gene-related peptide), which is released from a subset of activated primary afferents, is regarded as an important mediator. CGRP is not only a potent vasodilator but is also involved in nociceptive transmission in the trigeminal nucleus. Inhibition of CGRP receptors by the high-affinity CGRP receptor antagonist BIBN4096BS, which had proved its therapeutic potency in migraine patients, led to a significant decrease in neuronal activity in the spinal trigeminal nucleus of the rat. Another important vasodilatory mediator in meningeal nociception seems to be nitric oxide (NO), which may facilitate CGRP release from peripheral and central trigeminal structures. Inhibition of NO generation was effective in lowering the neuronal activity in the spinal trigeminal nucleus as well, whereas infusion of NO donors led to an increase in activity. The activiation showed typically a biphasic pattern. The delayed response can only be explained by secondary processes such as the expression of pro-nociceptive substances in the trigeminal nucleus or ganglion, as indicated by preliminary experimental studies. The fact that clinical and basic experimental data complement each other highlights the interpretative value of basic experiments for the pathophysiological mechanisms underlying the generation of headaches.",
keywords = "BIBN4096BS, CGRP, Headache, Nitric oxide, Trigeminovascular system",
author = "Karl Me{\ss}linger and {De Col}, R. and T. Denekas and M. Dux and M. Eberhardt and Koulchitsky, {S. V.} and J. R{\"o}der and Schlechtweg, {P. M.} and Sixt, {M. L.} and N. Schwenger and T. Strecker and M. Tr{\"o}ltzsch and Fischer, {M. J M}",
year = "2007",
month = "11",
doi = "10.1055/s-2007-970952",
language = "German",
volume = "34",
pages = "504--507",
journal = "Aktuelle Neurologie",
issn = "0302-4350",
publisher = "Georg Thieme Verlag",
number = "9",

}

TY - JOUR

T1 - Mediatorwirkungen im trigeminovaskulären system als grundlage für die nozizeptiven vorgänge bei der kopfschmerzentstehung

AU - Meßlinger, Karl

AU - De Col, R.

AU - Denekas, T.

AU - Dux, M.

AU - Eberhardt, M.

AU - Koulchitsky, S. V.

AU - Röder, J.

AU - Schlechtweg, P. M.

AU - Sixt, M. L.

AU - Schwenger, N.

AU - Strecker, T.

AU - Tröltzsch, M.

AU - Fischer, M. J M

PY - 2007/11

Y1 - 2007/11

N2 - Nociceptive mechanisms in the trigeminovascular system are probably involved in the generation of different forms of hedaches, wherein the neuropeptide CGRP (calcitonin gene-related peptide), which is released from a subset of activated primary afferents, is regarded as an important mediator. CGRP is not only a potent vasodilator but is also involved in nociceptive transmission in the trigeminal nucleus. Inhibition of CGRP receptors by the high-affinity CGRP receptor antagonist BIBN4096BS, which had proved its therapeutic potency in migraine patients, led to a significant decrease in neuronal activity in the spinal trigeminal nucleus of the rat. Another important vasodilatory mediator in meningeal nociception seems to be nitric oxide (NO), which may facilitate CGRP release from peripheral and central trigeminal structures. Inhibition of NO generation was effective in lowering the neuronal activity in the spinal trigeminal nucleus as well, whereas infusion of NO donors led to an increase in activity. The activiation showed typically a biphasic pattern. The delayed response can only be explained by secondary processes such as the expression of pro-nociceptive substances in the trigeminal nucleus or ganglion, as indicated by preliminary experimental studies. The fact that clinical and basic experimental data complement each other highlights the interpretative value of basic experiments for the pathophysiological mechanisms underlying the generation of headaches.

AB - Nociceptive mechanisms in the trigeminovascular system are probably involved in the generation of different forms of hedaches, wherein the neuropeptide CGRP (calcitonin gene-related peptide), which is released from a subset of activated primary afferents, is regarded as an important mediator. CGRP is not only a potent vasodilator but is also involved in nociceptive transmission in the trigeminal nucleus. Inhibition of CGRP receptors by the high-affinity CGRP receptor antagonist BIBN4096BS, which had proved its therapeutic potency in migraine patients, led to a significant decrease in neuronal activity in the spinal trigeminal nucleus of the rat. Another important vasodilatory mediator in meningeal nociception seems to be nitric oxide (NO), which may facilitate CGRP release from peripheral and central trigeminal structures. Inhibition of NO generation was effective in lowering the neuronal activity in the spinal trigeminal nucleus as well, whereas infusion of NO donors led to an increase in activity. The activiation showed typically a biphasic pattern. The delayed response can only be explained by secondary processes such as the expression of pro-nociceptive substances in the trigeminal nucleus or ganglion, as indicated by preliminary experimental studies. The fact that clinical and basic experimental data complement each other highlights the interpretative value of basic experiments for the pathophysiological mechanisms underlying the generation of headaches.

KW - BIBN4096BS

KW - CGRP

KW - Headache

KW - Nitric oxide

KW - Trigeminovascular system

UR - http://www.scopus.com/inward/record.url?scp=36549087648&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=36549087648&partnerID=8YFLogxK

U2 - 10.1055/s-2007-970952

DO - 10.1055/s-2007-970952

M3 - Article

AN - SCOPUS:36549087648

VL - 34

SP - 504

EP - 507

JO - Aktuelle Neurologie

JF - Aktuelle Neurologie

SN - 0302-4350

IS - 9

ER -