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.

Plasma levels of calcitonin gene-related peptide in chronic tension-type headache

Neurology ◽  
2000 ◽  
Vol 55 (9) ◽  
pp. 1335-1340 ◽  
Author(s):  
M. Ashina ◽  
L. Bendtsen ◽  
R. Jensen ◽  
S. Schifter ◽  
I. Jansen-Olesen ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Calcitonin Gene Related Peptide ◽  
Tension Type Headache ◽  
Chronic Tension Type Headache ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Type Headache

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.

Glyceryl Trinitrate may Trigger Endogenous Nitric Oxide Production in Patients with Chronic Tension-Type Headache

Cephalalgia ◽  
2004 ◽  
Vol 24 (11) ◽  
pp. 967-972 ◽  
Author(s):  
M Ashina ◽  
H Simonsen ◽  
L Bendtsen ◽  
R Jensen ◽  
J Olesen
Keyword(s):  
Nitric Oxide ◽  
Glyceryl Trinitrate ◽  
Plasma Levels ◽  
Experimental Studies ◽  
Tension Type Headache ◽  
Primary Headaches ◽  
No Production ◽  
Chronic Tension Type Headache ◽  
Endogenous Production ◽  
Type Headache

Experimental studies in humans have shown that nitric oxide (NO) may play an important role in initiation of primary headaches. It has been proposed that activation of L-arginine-NO pathway and increased endogenous production of NO may be responsible for NO induced headache. NO is synthesized from L-arginine and that reaction also yields citrulline. In the present study we aimed to investigate plasma levels of citrulline and arginine as markers of NO production after infusion of the NO donor, glyceryl trinitrate (GTN). We recruited 16 patients with chronic tension-type headache and 16 healthy controls. The subjects were randomly allocated to receive 0.5 μg/kg/min GTN or placebo over 20 min. Patients were examined on headache free days. Blood samples were collected at baseline and 60 min after start of infusion. Both patients and controls developed stronger immediate headache on the GTN day than on the placebo day ( P = 0.008). The headache was more pronounced in patients than in controls ( P = 0.02). Plasma levels of citrulline increased significantly 60 min after start of GTN infusion compared to placebo infusion in patients ( P = 0.01) but not in controls ( P = 0.50). Plasma levels of arginine were unchanged in both patients ( P = 0.12) and controls ( P =0.18). We suggest that GTN administration may trigger endogenous production of NO in patients with chronic tension-type headache resulting in activation of perivascular sensory afferents.

scholarly journals CGRP measurements in human plasma – a methodological study

Cephalalgia ◽  
2021 ◽  
pp. 033310242110241
Author(s):  
Karl Messlinger ◽  
Birgit Vogler ◽  
Annette Kuhn ◽  
Julika Sertel-Nakajima ◽  
Florian Frank ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Calcitonin Gene Related Peptide ◽  
Enzyme Linked Immunosorbent Assay ◽  
Published Data ◽  
Human Blood Plasma ◽  
Primary Headaches ◽  
Peptidase Inhibitors ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Standard Solutions

Background Calcitonin gene-related peptide plasma levels have frequently been determined as a biomarker for primary headaches. However, published data is often inconsistent resulting from different methods that are not precisely described in most studies. Methods We applied a well-proven enzyme-linked immunosorbent assay to measure calcitonin gene-related peptide concentrations in human blood plasma, we modified parameters of plasma preparation and protein purification and used calcitonin gene-related peptide-free plasma for standard solutions, which are described in detail. Results Calcitonin gene-related peptide levels are stable in plasma with peptidase inhibitors and after deep-freezing. Calcitonin gene-related peptide standard solutions based on synthetic intercellular fluid or pooled plasma with pre-absorbed calcitonin gene-related peptide influenced the measurements but yielded both comprehensible results. In a sample of 56 healthy subjects the calcitonin gene-related peptide plasma levels varied considerably from low (<50 pg/mL) to very high (>500 pg/mL) values. After a 12-hour exposure of these subjects to normobaric hypoxia the individual calcitonin gene-related peptide levels remained stable. Conclusion Buffering with peptidase inhibitors and immediate freezing or processing of plasma samples is essential to achieve reliable measurements. Individuals show considerable differences and partly high calcitonin gene-related peptide plasma levels without detectable pathological reason. Thus plasma measurements are suited particularly to follow calcitonin gene-related peptide levels in longitudinal studies. The use of data for this study was approved by the Ethics Committee of the Medical University of Innsbruck ( https://www.i-med.ac.at/ethikkommission/ ; EK Nr: 1242/2017).

Organ culture of the trigeminal ganglion induces enhanced expression of calcitonin gene-related peptide via activation of extracellular signal-regulated protein kinase 1/2

Cephalalgia ◽  
2010 ◽  
Vol 31 (1) ◽  
pp. 95-105 ◽  
Author(s):  
János Tajti ◽  
Anikó Kuris ◽  
László Vécsei ◽  
Cang-Bao Xu ◽  
Lars Edvinsson
Keyword(s):  
Protein Kinase ◽  
Organ Culture ◽  
Glial Cells ◽  
Calcitonin Gene Related Peptide ◽  
Trigeminal Ganglia ◽  
Primary Headaches ◽  
Related Peptide ◽  
Extracellular Signal ◽  
Calcitonin Gene

Background and objective: Clinical and experimental studies have revealed a central role of calcitonin gene-related peptide (CGRP) in primary headaches. The role of extracellular signal-regulated kinase 1 and 2 (ERK1/2) in neuronal and glial cell expression of CGRP- immunoreactivity (-ir) in rat trigeminal ganglia was studied with an organ culture method. Experimental procedures: Sections of adult rat trigeminal ganglia were cultured for up to 48 hours, examined with immunohistochemistry and quantitative real-time polymerase chain reaction (PCR) assay. Specific antibodies against CGRP, phosphorylated ERK1/2 (pERK1/2), total ERK1/2 (tERK1/2), phosphorylated p38 (pp38), phosphorylated C-Jun-N-terminal protein kinase (pJNK), pro-calcitonin (pro-CT), CGRP receptor activity modifying protein 1 (RAMP1), glutamine synthetase (GS) and pro-CT were used. To explore molecular mechanisms involved in the organ culture–induced CGRP-ir in neurons and glial cells, the effects of the MEK/ERK1/2 inhibitor U0126, its inactive analogue U0124, the p38 inhibitor SB203580 and the JNK inhibitor SP600125 were studied. Results: In fresh ganglia, small- and medium-sized neurons were CGRP-ir while some larger neurons displayed RAMP1-ir. Glial cells were negative to both. After organ culture, neurons showed enhanced CGRP- and RAMP1-ir. In addition, some glial cells were RAMP1- and CGRP-ir. Isolated glial cells and neurons were found to contain CGRP mRNA, and showed pro-CT-ir, suggestive of local formation of CGRP. Neurons and glial cells showed enhanced pERK1/2-ir already after two hours of organ culture and this remained elevated for 48 hours. There was transient pJNK-ir in neurons at two hours, while pp38-ir was not altered. U0126 reduced the enhanced pERK1/2-ir, while U0124 had no such effect; the CGRP-ir in neurons and glial cells was reduced at 48 hours and in parallel the CGRP mRNA expression was lower at 24 hours. Conclusion: We suggest that in conditions of elevated CGRP expression, inhibition of ERK1/2 might be an option for novel treatment.

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