scholarly journals Role Of Cgrp In Sensitization Of Dura Mater

2001 ◽  
Vol 1 ◽  
pp. 20-20
Author(s):  
K. Messlinger
Keyword(s):  
Dura Mater ◽  
Trigeminal Nerve ◽  
Plasma Levels ◽  
Nerve Fibers ◽  
Considerable Proportion ◽  
Trigeminovascular System ◽  
Dura Mater Encephali ◽  
Related Peptide ◽  
Calcitonin Gene

The mammalian dura mater encephali is richly supplied by trigeminal nerve fibers, a considerable proportion of which contains calcitonin gene-related peptide (CGRP). As plasma levels of CGRP are increased in some forms of headaches, the question is in which way CGRP is involved in nociceptive mechanisms within the peripheral and the central trigeminovascular system.

Calcitonin gene related peptide released from dural nerve fibers mediates increase of meningeal blood flow in the rat

1995 ◽  
Vol 73 (7) ◽  
pp. 1020-1024 ◽  
Author(s):  
K. Meßlinger ◽  
U. Hanesch ◽  
M. Kurosawa ◽  
M. Pawlak ◽  
R. F. Schmidt
Keyword(s):  
Blood Flow ◽  
Dura Mater ◽  
Calcitonin Gene Related Peptide ◽  
Nerve Fibers ◽  
Dura Mater Encephali ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Meningeal Blood Flow ◽  
Meningeal Artery ◽  
Stimulation Of

The parietal dura mater encephali of the rat was shown by immunohistochemistry to be densely innervated by calcitonin gene related peptide (CGRP) immunoreactive nerve fibers spreading around the medial meningeal artery and its branches. Electrical stimulation of the dural surface (10–20 V, 5–10 Hz, 10–30 min) caused a depletion of CGRP-immunopositive fibers, suggesting a release of CGRP. The dural blood flow around branches of the medial meningeal artery was also monitored with a laser Doppler flowmeter. Short periods (30 s) of electrical stimulation with parameters that presumably released CGRP from nerve fibers caused a repeatable and constant increase of the blood flow for 1–2 min. This evoked increase could dose dependently be inhibited by topical application of the CGRP antagonist hCGRP8–37. Accordingly, administration of hCGRP increased the basal blood flow. We conclude that stimulation of trigeminal afferents innervating the dura mater releases CGRP from peptidergic afferent terminals, thereby causing vasodilatation and increasing the meningeal blood flow, an important element of neurogenic inflammation.Key words: dura mater encephali, afferent nerve fibers, calcitonin gene related peptide, immunohistochemistry, laser Doppler flowmetry.

scholarly journals Calcitonin Gene-Related Peptide in Tension-Type Headache

2002 ◽  
Vol 2 ◽  
pp. 1527-1531 ◽  
Author(s):  
M. Ashina
Keyword(s):  
Plasma Levels ◽  
Calcitonin Gene Related Peptide ◽  
Tension Type Headache ◽  
Nerve Fibers ◽  
Primary Headaches ◽  
Chronic Tension Type Headache ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Type Headache

In the last 10 years there has been increasing interest in the role of calcitonin gene-related peptide (CGRP) in primary headaches. Tension-type headache is one of the most common and important types of primary headaches, and ongoing nociception from myofascial tissues may play an important role in the pathophysiology of this disorder. CGRP sensory fibers are preferentially located in the walls of arteries, and nerve fibers containing CGRP accompany small blood vessels in human cranial muscles. It is well established that nociception may lead to release of CGRP from sensory nerve endings and from central terminals of sensory afferents into the spinal cord. It has also been shown that density of CGRP fibers around arteries is increased in persistently inflamed muscle. These findings indicate that ongoing activity in sensory neurons in the cranial muscles may be reflected in changes of plasma levels of neuropeptides in patients with chronic tension-type headache. To explore the possible role of CGRP in tension-type headache, plasma levels of CGRP were measured in patients with chronic tension-type headache. This study showed that plasma levels of CGRP are normal in patients and unrelated to headache state. However, the findings of normal plasma levels of CGRP do not exclude the possibility that abnormalities of this neuropeptide at the neuronal or peripheral (pericranial muscles) levels play a role in the pathophysiology of tension-type headache. Investigation of CGRP in other compartments with new sensitive methods of analysis is necessary to clarify its role in tension-type headache.

Oxytocin as a regulatory neuropeptide in the trigeminovascular system: Localization, expression and function of oxytocin and oxytocin receptors

Cephalalgia ◽  
2020 ◽  
Vol 40 (12) ◽  
pp. 1283-1295
Author(s):  
Karin Warfvinge ◽  
Diana N Krause ◽  
Aida Maddahi ◽  
Anne-Sofie Grell ◽  
Jacob CA Edvinsson ◽  
...  
Keyword(s):  
Dura Mater ◽  
Calcitonin Gene Related Peptide ◽  
Trigeminal Ganglia ◽  
Trigeminal Nucleus ◽  
Trigeminovascular System ◽  
Related Peptide ◽  
Oxytocin Receptors ◽  
Calcitonin Gene ◽  
And Function ◽  
Cranial Arteries

Background Recent clinical findings suggest that oxytocin could be a novel treatment for migraine. However, little is known about the role of this neuropeptide/hormone and its receptor in the trigeminovascular pathway. Here we determine expression, localization, and function of oxytocin and oxytocin receptors in rat trigeminal ganglia and targets of peripheral (dura mater and cranial arteries) and central (trigeminal nucleus caudalis) afferents. Methods The methods include immunohistochemistry, messenger RNA measurements, quantitative PCR, release of calcitonin gene-related peptide and myography of arterial segments. Results Oxytocin receptor mRNA was expressed in rat trigeminal ganglia and the receptor protein was localized in numerous small to medium-sized neurons and thick axons characteristic of A∂ sensory fibers. Double immunohistochemistry revealed only a small number of neurons expressing both oxytocin receptors and calcitonin gene-related peptide. In contrast, double immunostaining showed expression of the calcitonin gene-related peptide receptor component receptor activity-modifying protein 1 and oxytocin receptors in 23% of the small cells and in 47% of the medium-sized cells. Oxytocin immunofluorescence was observed only in trigeminal ganglia satellite glial cells. Oxytocin mRNA was below detection limit in the trigeminal ganglia. The trigeminal nucleus caudalis expressed mRNA for both oxytocin and its receptor. K+-evoked calcitonin gene-related peptide release from either isolated trigeminal ganglia or dura mater and it was not significantly affected by oxytocin (10 µM). Oxytocin directly constricted cranial arteries ex vivo (pEC50 ∼ 7); however, these effects were inhibited by the vasopressin V1A antagonist SR49059. Conclusion Oxytocin receptors are extensively expressed throughout the rat trigeminovascular system and in particular in trigeminal ganglia A∂ neurons and fibers, but no functional oxytocin receptors were demonstrated in the dura and cranial arteries. Thus, circulating oxytocin may act on oxytocin receptors in the trigeminal ganglia to affect nociception transmission. These effects may help explain hormonal influences in migraine and offer a novel way for treatment.

scholarly journals Anorectic effect of amylin is not transmitted by capsaicin-sensitive nerve fibers

1998 ◽  
Vol 274 (6) ◽  
pp. R1777-R1782 ◽  
Author(s):  
Thomas A. Lutz ◽  
Janine Althaus ◽  
Rinaldo Rossi ◽  
Erwin Scharrer
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Area Postrema ◽  
Nerve Fibers ◽  
Solitary Tract ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Anorectic Effect ◽  
The Central Nervous System

Abdominal vagal and splanchnic afferents play an important role in the control of food intake in that they transmit various satiety signals to the central nervous system. Inasmuch as previous studies have shown that the anorectic effect of intraperitoneally injected amylin was not abolished by subdiaphragmatic vagotomy, the aim of the present study was to elucidate the role of splanchnic afferents in mediating amylin’s anorectic effect after intraperitoneal injection. Rats were pretreated intraperitoneally with the neurotoxin capsaicin, which destroys primary sensory (vagal and splanchnic) afferents. Sham-treated rats served as control. Capsaicin-pretreatment had no influence on the anorectic effects of amylin (5 μg/kg) and the related peptide, calcitonin gene-related peptide (CGRP; 5 μg/kg), in 24-h food-deprived rats. Abolition of cholecystokinin’s (3 μg/kg) anorectic effect agrees with previous studies and confirmed the effectiveness of the capsaicin pretreatment. In conclusion, the anorectic effects of intraperitoneally injected amylin and CGRP are not mediated by capsaicin-sensitive primary sensory neurons. Both anorectic peptides are, therefore, most likely to act within the central nervous system. Previous studies suggest that the relevant receptors might be located in neurons of the area postrema-nucleus of the solitary tract region.

Sign in / Sign up

Export Citation Format

Share Document