Reduction of Calcitonin Gene-Related Peptide in Jugular Blood Following Electrical Stimulation of Rat Greater Occipital Nerve

Cephalalgia ◽  
1992 ◽  
Vol 12 (5) ◽  
pp. 275-279 ◽  
Author(s):  
Maurice B Vincent ◽  
Rolf Ekman ◽  
Lars Edvinsson ◽  
Trond Sand ◽  
Ottar Sjaastad
Keyword(s):  
Electrical Stimulation ◽  
Calcitonin Gene Related Peptide ◽  
Trigeminal System ◽  
Occipital Nerve ◽  
Related Peptide ◽  
System Reduction ◽  
Calcitonin Gene ◽  
Greater Occipital Nerve ◽  
Ocular Signs ◽  
Stimulation Of

Although it is known that pain in the forehead may be induced by neck abnormalities, the actual neck-head connections responsible for development of pain in trigeminal areas are poorly understood. Vasoactive neuropeptides released from sensory fibres, such as substance P (SP) and calcitonin gene-related peptide (CGRP), have been considered as important elements in headache pathophysiology. The levels of CGRP-like immunoreactivity (LI) were measured bilaterally in the jugular blood (52 rats) and intraocular aspirates (66 rats) following electrical stimulation of the left greater occipital nerve, and in the jugular blood of 13 control animals. One-third of the stimulated rats had varying combinations of conjunctival injection, tearing, diminished eye aperture and miosis or mydriasis on the stimulated side. The other two-thirds exhibited no ocular signs. Significantly lower levels of CGRP-LI were present in the jugular blood on the stimulated side in comparison with control rats. There was comparatively lower CGRP-LI on the non-stimulated side as well, but to a lesser extent. Significant differences between the stimulated and the non-stimulated side were present, particularly in the tearing/diminished eye cleft group. It is proposed that stimulation of the rat GON inhibits the trigeminal system (reduction of CGRP-LI) and possibly activates parasympathetic fibres (ocular changes).

scholarly journals Effect of Ultrasound Guided Bilateral Greater Occipital Nerve Block on Serum Calcitonin Gene Related Peptide (CGRP) in Chronic Migraine

2021 ◽  
Vol 10 (1) ◽  
pp. 01-05
Author(s):  
Abdelrahman Atef ◽  
Mahmoud Haroun ◽  
Ali Soliman ◽  
Ramez Mostafa ◽  
Ahmed Elsadek ◽  
...  
Keyword(s):  
Chronic Migraine ◽  
Nerve Block ◽  
Calcitonin Gene Related Peptide ◽  
Ultrasound Guided ◽  
Occipital Nerve ◽  
Related Peptide ◽  
Greater Occipital Nerve Block ◽  
Calcitonin Gene ◽  
Greater Occipital Nerve ◽  
Occipital Nerve Block

Background: The trigeminal ganglion plays a key role in primary headache pathophysiology. Calcitonin gene-related peptide (CGRP) and CGRP receptors are expressed in trigeminal neurons that form C-fibers and A-fibers, respectively. In migraine attacks, there is release of CGRP into the cranial venous outflow, in refractory headache to conventional pharmacologic management, minimally invasive techniques such as greater occipital nerve block (GONB) are feasible for pain relief, and help to decrease the frequency of the attacks, Studies on the ultrasound (US) guided GON injection technique have emphasized that this technique has a higher success rate and should allow for a more precise block of the nerve. Our study will be concerned by correlation of CGRP level as a biomarker for effectiveness and responders of us guided GON block in chronic migraine (CM). Methods: twenty patients diagnosed with chronic migraine were recruited in this study. All participants underwent ultrasound-guided bilat. GONB by 40 mg triamcinolone and 1 cc leidocaine using a portable ultrasound system with a 7 – 13 MHz multifrequency transducer, blood samples were collected from antecubital vein immediately before and three to five weeks after injection clinical response was evaluated using headache diaries Results: CGRP levels after ultrasound guided GONB (median, 40 pg/mL; range, 25-60) were significantly lower as compared with CGRP levels obtained before GONB (median, 145 pg/mL; range, 60-380; P =0.001). Pretreatment CGRP levels in non-responders (310 pg/mL) were significantly higher than those seen in responders being in poor responders less than 50% improvement (135 pg/ml) and good responders (140 pg/mL; P = 0.003). One month after treatment. A number of demographic factors, clinical features, and comorbidities were not different in responders as compared with those of nonresponders. Conclusion: These results suggests that interictal CGRP levels can be of help in predicting the response to GONB and suggest that the mechanism of action of GONB in CM is the reversal of sensitization as a result of the inhibition of CGRP release still more studies needed to highlight CGRP role with GONB

scholarly journals Calcitonin gene-related peptide receptor antagonist human CGRP-(8-37)

1989 ◽  
Vol 256 (2) ◽  
pp. E331-E335 ◽  
Author(s):  
T. Chiba ◽  
A. Yamaguchi ◽  
T. Yamatani ◽  
A. Nakamura ◽  
T. Morishita ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Adenylate Cyclase ◽  
Calcitonin Gene Related Peptide ◽  
Human Calcitonin ◽  
Liver Plasma Membrane ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Liver Membranes ◽  
Calcitonin Receptors ◽  
Stimulation Of

From this study, we predicted that the human calcitonin gene-related peptide (hCGRP) fragment hCGRP-(8-37) would be a selective antagonist for CGRP receptors but an agonist for calcitonin (CT) receptors. In rat liver plasma membrane, where CGRP receptors predominate and CT appears to act through these receptors, hCGRP-(8-37) dose dependently displaced 125I-[Tyr0]rat CGRP binding. However, hCGRP-(8-37) had no effect on adenylate cyclase activity in liver plasma membrane. Furthermore, hCGRP-(8-37) inhibited adenylate cyclase activation induced not only by hCGRP but also by hCT. On the other hand, in LLC-PK1 cells, where calcitonin receptors are abundant and CGRP appears to act via these receptors, the bindings of 125I-[Tyr0]rat CGRP and 125I-hCT were both inhibited by hCGRP-(8-37). In contrast to liver membranes, interaction of hCGRP-(8-37) with these receptors led to stimulation of adenosine 3',5'-cyclic monophosphate (cAMP) production in LLC-PK1 cells, and moreover, this fragment did not inhibit the increased production of cAMP induced not only by hCT but also by hCGRP. Thus hCGRP-(8-37) appears to be a useful tool for determining whether the action of CGRP as well as that of CT is mediated via specific CGRP receptors or CT receptors.

Stimulation of acetylcholine release in myenteric plexus by calcitonin gene-related peptide

1990 ◽  
Vol 259 (6) ◽  
pp. G934-G939 ◽  
Author(s):  
M. W. Mulholland ◽  
S. Jaffer
Keyword(s):  
Myenteric Plexus ◽  
Acetylcholine Release ◽  
Calcitonin Gene Related Peptide ◽  
Ach Release ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Dependent Mechanism ◽  
Stimulation Of

The effects of calcitonin gene-related peptide (CGRP) on acetylcholine (ACh) release from myenteric plexus neurons in primary culture were investigated. CGRP (10(-12) to 10(-6) M) produced a dose-dependent increase in [3H]ACh release. The ACh release caused by CGRP was significantly inhibited (74 +/- 24%) by preincubation with dideoxyadenosine but was increased more than threefold by preincubation with theophylline. Incubation of myenteric plexus neurons with CGRP (10(-8) M) in the presence of diltiazem (10(-5) M) or in a calcium-free medium markedly reduced [3H]ACh release. CGRP potentiated [3H]ACh release stimulated by potassium or substance P but not by cholecystokinin octapeptide or forskolin. The results demonstrate that CGRP cause release of ACh from guinea pig myenteric plexus neurons and suggest that the peptide acts through an adenosine 3',5'-cyclic monophosphate-dependent mechanism that involves neuronal calcium channels.

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