scholarly journals A Pre-Existing Myogenic Temporomandibular Disorder Increases Trigeminal Calcitonin Gene-Related Peptide and Enhances Nitroglycerin-Induced Hypersensitivity in Mice

2020 ◽  
Vol 21 (11) ◽  
pp. 4049
Author(s):  
Hui Shu ◽  
Sufang Liu ◽  
Yuanyuan Tang ◽  
Brian L. Schmidt ◽  
John C. Dolan ◽  
...  
Keyword(s):  
Protein Level ◽  
Temporomandibular Disorder ◽  
Calcitonin Gene Related Peptide ◽  
Spinal Trigeminal Nucleus ◽  
Trigeminal Nucleus ◽  
Systemic Injection ◽  
Trigeminal Nucleus Caudalis ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Spinal Trigeminal Nucleus Caudalis

Migraine is commonly reported among patients with temporomandibular disorders (TMDs), especially myogenic TMD. The pathophysiologic mechanisms related to the comorbidity of the two conditions remain elusive. In the present study, we combined masseter muscle tendon ligation (MMTL)-produced myogenic TMD with systemic injection of nitroglycerin (NTG)-induced migraine-like hypersensitivity in mice. Facial mechanical allodynia, functional allodynia, and light-aversive behavior were evaluated. Sumatriptan, an FDA-approved medication for migraine, was used to validate migraine-like hypersensitivity. Additionally, we examined the protein level of calcitonin gene-related peptide (CGRP) in the spinal trigeminal nucleus caudalis using immunohistochemistry. We observed that mice with MMTL pretreatment have a prolonged NTG-induced migraine-like hypersensitivity, and MMTL also enabled a non-sensitizing dose of NTG to trigger migraine-like hypersensitivity. Systemic injection of sumatriptan inhibited the MMTL-enhanced migraine-like hypersensitivity. MMTL pretreatment significantly upregulated the protein level of CGRP in the spinal trigeminal nucleus caudalis after NTG injection. Our results indicate that a pre-existing myogenic TMD can upregulate NTG-induced trigeminal CGRP and enhance migraine-like hypersensitivity.

Calcitonin Gene-Related Peptide Receptor Inhibition Reduces Neuronal Activity Induced by Prolonged Increase in Nitric Oxide in the Rat Spinal Trigeminal Nucleus

Cephalalgia ◽  
2009 ◽  
Vol 29 (4) ◽  
pp. 408-417 ◽  
Author(s):  
S Kulchitsky ◽  
MJM Fischer ◽  
K Messlinger
Keyword(s):  
Nitric Oxide ◽  
Neuronal Activity ◽  
Calcitonin Gene Related Peptide ◽  
Primary Headaches ◽  
Spinal Trigeminal Nucleus ◽  
Trigeminal Nucleus ◽  
No Donors ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Tension Type Headaches

Infusion of nitric oxide (NO) donors is known to induce delayed attacks of migraine and cluster headache or aggravate tension-type headaches in patients suffering from these primary headaches. Previously we have reported that infusion of NO donors in the rat causes delayed neuronal activity in the spinal trigeminal nucleus, which parallels the above clinical observations. Suggesting that endogenous NO production is involved in the generation of primary headaches, we used this animal model of meningeal nociception to determine whether a prolonged increase in NO levels causes an increase in neuronal activity. In anaesthetized rats spinal trigeminal neurons with afferent input from the exposed dura were recorded. Continuous intravenous infusion of the NO donors sodium nitroprusside (25 μg/kg/h) or glycerol trinitrate (250 μg/ kg/h) for 2h induced a persisting increase in neuronal activity but no change in systemic blood pressure. In this activated trigeminal system the calcitonin gene-related peptide (CGRP) receptor antagonist BIBN4096BS (900 μg/ kg) was infused. Spinal trigeminal activity was significantly reduced within minutes and to a similar extent as previously reported in animals not treated with NO. Slow continuous NO infusion may be a model of the active headache phase, and inhibition of CGRP receptors can reverse the induced neuronal activity.

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