scholarly journals Calcitonin gene-related peptide in migraine: intersection of peripheral inflammation and central modulation

2011 ◽  
Vol 13 ◽  
Author(s):  
Ann C. Raddant ◽  
Andrew F. Russo
Keyword(s):  
Clinical Evidence ◽  
Wide Distribution ◽  
Calcitonin Gene Related Peptide ◽  
Protein Extravasation ◽  
Related Peptide ◽  
Plasma Protein Extravasation ◽  
Calcitonin Gene ◽  
Initial Activation ◽  
Local Release ◽  
The Brain

Over the past two decades, a convergence of basic and clinical evidence has established the neuropeptide calcitonin-gene-related peptide (CGRP) as a key player in migraine. Although CGRP is a recognised neuromodulator of nociception, its mechanism of action in migraine remains elusive. In this review, we present evidence that led us to propose that CGRP is well poised to enhance neurotransmission in migraine by both peripheral and central mechanisms. In the periphery, it is thought that local release of CGRP from the nerve endings of meningeal nociceptors following their initial activation by cortical spreading depression is critical for the induction of vasodilation, plasma protein extravasation, neurogenic inflammation and the consequential sensitisation of meningeal nociceptors. Mechanistically, we propose that CGRP release can give rise to a positive-feedback loop involved in localised increased synthesis and release of CGRP from neurons and a CGRP-like peptide called procalcitonin from trigeminal ganglion glia. Within the brain, the wide distribution of CGRP and CGRP receptors provides numerous possible targets for CGRP to act as a neuromodulator.

scholarly journals Role of Calcitonin Gene Related Peptide (CGRP) in Migraine

2017 ◽  
Vol 33 (1) ◽  
pp. 39-43
Author(s):  
Md Ashraf Ali ◽  
Habibur Rahaman
Keyword(s):  
Family Relationships ◽  
Preventive Treatment ◽  
Primary Headache ◽  
Calcitonin Gene Related Peptide ◽  
Childhood And Adolescence ◽  
Protein Extravasation ◽  
Related Peptide ◽  
Plasma Protein Extravasation ◽  
Calcitonin Gene ◽  
Potent Vasodilator

Migraine is the second most primary headache. The prevalence of Migraine is 12% in the general population, including 18% in women and 6% in men. Migraine can start in childhood and adolescence and continue throughout lifespan. It is most prevalent among people in their 30s and 40s. Migraine is a debilitating hemicranial headache that is pulsating, aggravated by movement, nausea, vomiting and having sensitivity to light and sound, with or without aura. It can affect all aspects of life as work and school, parenting and family relationships and personal and leisure time. There are some theory regarding pathogenesis of migraine which includes cortical spreading depression, cortical spreading oligemia, activation of trigeminocervical complex leading to neuroinflammation & release of vasodialating neuropeptides which include calcitonin gene related peptide (CGRP), substance P, vasoactive intestinal polypeptide (VIP), nitric oxide (NO), and pituitary adenylate cyclase activating peptide (PACAP) & genetic factor. CGRP is a potent vasodilator and causes perivascular plasma protein extravasation and nociceptive pain. Newer medications target CGRP both for acute and preventive treatment of migraine. Bangladesh Journal of Neuroscience 2017; Vol.  33 (1): 39-43

Distribution of calcitonin gene-related peptide-like immunoreactivity in the brain of the lizardPodarcis hispanica

2002 ◽  
Vol 447 (2) ◽  
pp. 99-113 ◽  
Author(s):  
Fernando Martínez-García ◽  
Amparo Novejarque ◽  
José M. Landete ◽  
Jose Moncho-Bogani ◽  
Enrique Lanuza
Keyword(s):  
Calcitonin Gene Related Peptide ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
The Brain

Calcitonin Gene-Related Peptide in the Brain, Spinal Cord, and Some Peripheral Systems

1992 ◽  
Vol 657 (1 Calcitonin Ge) ◽  
pp. 119-134 ◽  
Author(s):  
TOMAS HÖKFELT ◽  
ULF ARVIDSSON ◽  
SANDRA CECCATELLI ◽  
ROSER CORTÉS ◽  
STAFFAN CULLHEIM ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Calcitonin Gene Related Peptide ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
The Brain

Nicotine and acetylcholine induce release of calcitonin gene-related peptide from rat trachea

1994 ◽  
Vol 76 (4) ◽  
pp. 1651-1656 ◽  
Author(s):  
S. Jinno ◽  
X. Y. Hua ◽  
T. L. Yaksh
Keyword(s):  
Prolonged Exposure ◽  
Significant Degree ◽  
Calcitonin Gene Related Peptide ◽  
Related Peptide ◽  
Cgrp Release ◽  
Calcitonin Gene ◽  
Airway Responses ◽  
Local Release ◽  
Rat Trachea ◽  
Afferent Terminals

In the present study, we observed that nicotine, the nicotinic analogue cytisine, and acetylcholine (ACh) evoked a concentration-dependent (5 x 10(-6)-5 x 10(-5) M) release of calcitonin gene-related peptide (CGRP) from the rat trachea. After a prolonged exposure to capsaicin, nicotine-induced CGRP release was absent, suggesting that the release of CGRP by nicotine is derived from capsaicin-sensitive afferent terminals. Nicotine- and cytisine-induced release displayed a significant degree of tachyphylaxis after sequential exposures. The release of CGRP evoked by capsaicin was also reduced after nicotine and cytisine desensitization. This indicates that similar mechanisms may mediate the tachyphylactic effect of capsaicin and nicotine. Hexamethonium and mecamylamine blocked the effect of nicotine but not that of ACh, whereas atropine significantly attenuated the release of CGRP outflow induced by ACh. Physostigmine and neostigmine did not alter resting release of CGRP from rat trachea, although exogenous (10(-5) M) ACh-induced CGRP release was enhanced in the presence of neostigmine, suggesting minimal tonic cholinergic activity in this model. We conclude that activation of nicotinic and muscarinic receptors in the rat trachea can induce local release of CGRP. These observations indicate that cholinergically induced airway responses may be mediated in part by activation of the peripheral terminals of primary afferent sensory neurons and subsequent release of local neuropeptides.

Effects of calcitonin gene-related peptide on rat soleus muscle excitability: mechanisms and physiological significance

2008 ◽  
Vol 295 (4) ◽  
pp. R1214-R1223 ◽  
Author(s):  
W. A. Macdonald ◽  
O. B. Nielsen ◽  
T. Clausen
Keyword(s):  
Calcitonin Gene Related Peptide ◽  
Resting Membrane Potential ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Rat Soleus Muscle ◽  
Force Recovery ◽  
Initial Force ◽  
Local Release ◽  
Muscle Excitability

Intense exercise causes a large loss of K+ from contracting muscles. The ensuing elevation of extracellular K+ ([K+]o) has been suggested to cause fatigue by depressing muscle fiber excitability. In isolated muscles, however, repeated contractions confer some protection against this effect of elevated K+. We hypothesize that this excitation-induced force-recovery is related to the release of the neuropeptide calcitonin gene-related peptide (CGRP), which stimulates the muscular Na+-K+ pumps. Using the specific CGRP antagonist CGRP-(8-37), we evaluated the role of CGRP in the excitation-induced force recovery and examined possible mechanisms. Intact rat soleus muscles were stimulated to evoke short tetani at regular intervals. Increasing extracellular K+ ([K+]o) from 4 to 11 mM decreased force to ∼20% of initial force ( P < 0.001). Addition of exogenous CGRP (10−9 M), release of endogenous CGRP with capsaicin, or repeated electrical stimulation recovered force to 50–70% of initial force ( P < 0.001). In all cases, force recovery could be almost completely suppressed by CGRP-(8-37). At 11 mM [K+]o, CGRP (10−8 M) did not alter resting membrane potential or conductance but significantly improved action potentials ( P < 0.001) and increased the proportion of excitable fibers from 32 to 70% ( P < 0.001). CGRP was shown to induce substantial force recovery with only modest Na+-K+ pump stimulation. We conclude that the excitation-induced force recovery is caused by a recovery of excitability, induced by local release of CGRP. The data suggest that the recovery of excitability partly was induced by Na+-K+ pump stimulation and partly by altering Na+ channel function.

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