scholarly journals A novel CGRP-neutralizing Spiegelmer attenuates neurogenic plasma protein extravasation

2015 ◽  
Vol 172 (12) ◽  
pp. 3086-3098 ◽  
Author(s):  
K Hoehlig ◽  
K W Johnson ◽  
E Pryazhnikov ◽  
C Maasch ◽  
A Clemens-Smith ◽  
...  
Keyword(s):  
Plasma Protein ◽  
Protein Extravasation ◽  
Plasma Protein Extravasation

Effects of Parecoxib on Plasma Protein Extravasation and c-Fos Expression in the Rat

2006 ◽  
Vol 46 (2) ◽  
pp. 276-285 ◽  
Author(s):  
Sigrid Schuh-Hofer ◽  
Mandana Tayefeh ◽  
Uwe Reuter ◽  
Ulrich Dirnagl ◽  
Guy Arnold
Keyword(s):  
Plasma Protein ◽  
Protein Extravasation ◽  
Plasma Protein Extravasation ◽  
Fos Expression

scholarly journals Investigation of 5-HT2B receptor induced dural plasma protein extravasation in a mouse migraine model

2013 ◽  
Vol 14 (S1) ◽  
Author(s):  
A Hunfeld ◽  
D Segelcke ◽  
M Andriske ◽  
F Paris ◽  
X Zhu ◽  
...  
Keyword(s):  
Plasma Protein ◽  
Protein Extravasation ◽  
Plasma Protein Extravasation

scholarly journals Hypoxia facilitates neurogenic dural plasma protein extravasation in mice: a novel animal model for migraine pathophysiology

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Anika Hunfeld ◽  
Daniel Segelcke ◽  
Ingo Bäcker ◽  
Badreddine Mecheri ◽  
Kathrin Hemmer ◽  
...  
Keyword(s):  
Animal Model ◽  
Plasma Protein ◽  
Protein Extravasation ◽  
Plasma Protein Extravasation ◽  
Migraine Pathophysiology

Evidence for 5-HT1B/1D Receptors Mediating the Antimigraine Effect of Sumatriptan and Dihydroergotamine

Cephalalgia ◽  
1991 ◽  
Vol 11 (4) ◽  
pp. 165-168 ◽  
Author(s):  
Maria Gabriella Buzzi ◽  
Michael A Moskowitz
Keyword(s):  
Trigeminal Ganglion ◽  
Dura Mater ◽  
Plasma Protein ◽  
Cell Activation ◽  
Rank Order ◽  
Plasma Extravasation ◽  
Protein Extravasation ◽  
Trigeminal Stimulation ◽  
Plasma Protein Extravasation ◽  
Pre Treatment

Neurogenic plasma extravasation, endothelial cell activation (increase in vesicle number and vacuole formation), platelet aggregation and adhesion, and mast cell degranulation occur selectively in postcapillary venules of the dura mater following electrical trigeminal ganglion stimulation, and are mediated by release of neuropeptides from perivascular unmyelinated C fibres. Pre-treatment with the antimigraine drugs dihydroergotamine and sumatriptan, two drugs that bind with high affinity to 5-HT1B/1D receptors, markedly attenuated plasma protein extravasation induced by electrical trigeminal ganglion stimulation. Trigeminal stimulation increased plasma calcitonin gene-related peptide levels in rat superior sagittal sinus. Pre-treatment with dihydroergotamine and, to a lesser extent, sumatriptan, attenuated this increase. Both drugs reduced morphological changes in post-capillary venules and mast cells within dura mater following electrical trigeminal ganglion stimulation. Plasma protein extravasation was selectively blocked in dura mater (but not in extracranial tissues) by pre-treatment with those receptor agonists showing a rank order of potency suggesting a 3-HT1B/1D interaction (5-CT > 5-BT > DHE > sumatriptan > 8-OH-DPAT). Pre-treatment with 5-HT2 and 5-HT3 antagonists was not effective. Taken together, these data are consistent with the interpretation that putative 5-HT-1B/1D receptors located on sensory fibres are coupled to inhibition of peptide release and blockade of neurogenic inflammation. An important therapeutic action of ergot alkaloids and sumatriptan in migraine headaches is so defined.

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