meningeal blood flow
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Cephalalgia ◽  
2021 ◽  
pp. 033310242198926
Author(s):  
Miklós Lengyel ◽  
Dominika Hajdu ◽  
Alice Dobolyi ◽  
Judit Rosta ◽  
Gábor Czirják ◽  
...  

Background TWIK-related spinal cord potassium channel (TRESK) background potassium channels have a key role in controlling resting membrane potential and excitability of sensory neurons. A frameshift mutation leading to complete loss of TRESK function has been identified in members of a family suffering from migraine with aura. In the present study, we examined the role of TRESK channels on nociceptor function in mice. Methods Calcium imaging was used to investigate the role of TRESK channels in the modulation of the response evoked by transient receptor potential vanilloid 1 (TRPV1) receptor stimulation in dorsal root ganglion neurons. Release of calcitonin gene-related peptide from trigeminal afferents and changes in meningeal blood flow were also measured. Experiments were performed on wild-type and TRESK knockout animals. Results Inhibition of TRESK increased the TRPV1-mediated calcium signal in dorsal root ganglion neurons and potentiated capsaicin-induced increases in calcitonin gene-related peptide release and meningeal blood flow. Activation of TRESK decreased the capsaicin sensitivity of sensory neurons, leading to an attenuation of capsaicin-induced increase in meningeal blood flow. In TRESK knockout animals, TRPV1-mediated nociceptive reactions were unaffected by pretreatment with TRESK modulators. Conclusions Pharmacological manipulation of TRESK channels influences the TRPV1-mediated functions of nociceptors. Altered TRESK function might contribute to trigeminal nociceptor sensitization in migraine patients.


2019 ◽  
Vol 24 (2) ◽  
pp. 383-397 ◽  
Author(s):  
Mária Dux ◽  
Alexandru Babes ◽  
Jessica Manchen ◽  
Julika Sertel‐Nakajima ◽  
Birgit Vogler ◽  
...  

Neuropeptides ◽  
2017 ◽  
Vol 65 ◽  
pp. 130
Author(s):  
Maria Dux ◽  
Christine Will ◽  
Birgit Vogler ◽  
Milos R. Filipovic ◽  
Karl Messlinger

2015 ◽  
Vol 173 (3) ◽  
pp. 431-445 ◽  
Author(s):  
Mária Dux ◽  
Christine Will ◽  
Birgit Vogler ◽  
Milos R Filipovic ◽  
Karl Messlinger

Cephalalgia ◽  
2015 ◽  
Vol 35 (13) ◽  
pp. 1192-1201 ◽  
Author(s):  
Phillip Edward Kunkler ◽  
LuJuan Zhang ◽  
Jessica Joan Pellman ◽  
Gerry Stephen Oxford ◽  
Joyce Harts Hurley

Background Air pollution is linked to increased emergency room visits for headache, and migraine patients frequently cite chemicals or odors as headache triggers, but the association between air pollutants and headache is not well understood. We previously reported that nasal administration of environmental irritants acutely increases meningeal blood flow via a TRPA1-dependent mechanism involving the trigeminovascular system. Here, we examine whether chronic environmental irritant exposure sensitizes the trigeminovascular system. Methods Male rats were exposed to acrolein, a TRPA1 agonist, or room air by inhalation for four days prior to meningeal blood flow measurements. Some animals were injected daily with a TRPA1 antagonist, AP-18, or vehicle prior to inhalation exposure. Trigeminal ganglia were isolated following blood flow measurements for immunocytochemistry and/or qPCR determination of TRPV1, TRPA1 and CGRP levels. Results Acrolein inhalation exposure potentiated blood flow responses both to TRPA1 and TRPV1 agonists compared to room air. Acrolein exposure did not alter TRPV1 or TRPA1 mRNA levels or TRPV1 or CGRP immunoreactive cell counts in the trigeminal ganglion. Acrolein sensitization of trigeminovascular responses to a TRPA1 agonist was attenuated by pre-treatment with AP-18. Interpretation These results suggest trigeminovascular sensitization as a mechanism for enhanced headache susceptibility after chemical exposure.


2013 ◽  
Vol 14 (S1) ◽  
Author(s):  
M Dux ◽  
M Eberhardt ◽  
MR Filipovic ◽  
R DeCol ◽  
K Messlinger

2013 ◽  
Vol 1 (Suppl 1) ◽  
pp. P88
Author(s):  
M Dux ◽  
M Eberhardt ◽  
MR Filipovic ◽  
R DeCol ◽  
K Messlinger

2006 ◽  
Vol 148 (4) ◽  
pp. 536-543 ◽  
Author(s):  
Thomas Denekas ◽  
Markus Tröltzsch ◽  
Axel Vater ◽  
Sven Klussmann ◽  
Karl Messlinger

2002 ◽  
Vol 137 (6) ◽  
pp. 874-880 ◽  
Author(s):  
Mária Dux ◽  
Nina Schwenger ◽  
Karl Messlinger

Cephalalgia ◽  
2002 ◽  
Vol 22 (3) ◽  
pp. 233-241 ◽  
Author(s):  
T Strecker ◽  
M Dux ◽  
K Messlinger

This study addresses possible interactions of the vasodilators nitric oxide (NO), calcitonin gene-related peptide (CGRP) and prostaglandins, which may be implicated in the generation of vascular headaches. Local application of the NO donator diethylamine-NONOate (NONOate) to the exposed dura mater encephali of the rat caused dose-dependent increases in meningeal blood flow recorded by laser Doppler flowmetry. Pre-application of the CGRP receptor antagonist CGRP8-37 significantly attenuated the evoked blood flow increases, while the cyclooxygenase inhibitors acetylsalicylic acid and metamizol were only marginally effective. Stimulation of rat dura mater with NONOate in vitro caused increases in CGRP release. NADPH- diaphorase activity indicating NO production was restricted to the endothelium of dural arterial vessels. We conclude that increases in meningeal blood flow caused by NO depend partly on the release and vasodilatory action of CGRP from dural afferents, while prostaglandins are not significantly involved.


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