scholarly journals Role of CGRP in Neuroimmune Interaction via NF-κB Signaling Genes in Glial Cells of Trigeminal Ganglia

2020 ◽  
Vol 21 (17) ◽  
pp. 6005
Author(s):  
Shaista Afroz ◽  
Rieko Arakaki ◽  
Takuma Iwasa ◽  
Arief Waskitho ◽  
Masamitsu Oshima ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Glial Cells ◽  
Inflammatory Responses ◽  
Trigeminal System ◽  
Spinal Trigeminal Nucleus ◽  
Trigeminal Nucleus ◽  
Array Analysis ◽  
Activation Markers ◽  
Neuroimmune Interaction ◽  
Trigeminal Nucleus Caudalis

Activation of the trigeminal system causes the release of various neuropeptides, cytokines, and other immune mediators. Calcitonin gene-related peptide (CGRP), which is a potent algogenic mediator, is expressed in the peripheral sensory neurons of trigeminal ganglion (TG). It affects the inflammatory responses and pain sensitivity by modulating the activity of glial cells. The primary aim of this study was to use array analysis to investigate the effect of CGRP on the glial cells of TG in regulating nuclear factor kappa B (NF-κB) signaling genes and to further check if CGRP in the TG can affect neuron-glia activation in the spinal trigeminal nucleus caudalis. The glial cells of TG were stimulated with CGRP or Minocycline (Min) + CGRP. The effect on various genes involved in NF-κB signaling pathway was analyzed compared to no treatment control condition using a PCR array analysis. CGRP, Min + CGRP or saline was directly injected inside the TG and the effect on gene expression of Egr1, Myd88 and Akt1 and protein expression of cleaved Caspase3 (cleav Casp3) in the TG, and c-Fos and glial fibrillary acidic protein (GFAP) in the spinal section containing trigeminal nucleus caudalis was analyzed. Results showed that CGRP stimulation resulted in the modulation of several genes involved in the interleukin 1 signaling pathway and some genes of the tumor necrosis factor pathway. Minocycline pre-treatment resulted in the modulation of several genes in the glial cells, including anti-inflammatory genes, and neuronal activation markers. A mild increase in cleav Casp3 expression in TG and c-Fos and GFAP in the spinal trigeminal nucleus of CGRP injected animals was observed. These data provide evidence that glial cells can participate in neuroimmune interaction due to CGRP in the TG via NF-κB signaling pathway.

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.

Enkephalin and substance P effects related to trigeminal pain

1978 ◽  
Vol 56 (2) ◽  
pp. 216-222 ◽  
Author(s):  
R. K. Andersen ◽  
J. P. Lund ◽  
E. Puil
Keyword(s):  
Substance P ◽  
Firing Frequency ◽  
Tooth Pulp ◽  
Trigeminal System ◽  
Noxious Stimulation ◽  
Spontaneous Firing ◽  
Trigeminal Nucleus ◽  
Nociceptive Neurons ◽  
Trigeminal Nucleus Caudalis ◽  
Temporal Aspects

Iontophoretic applications of enkephalin (20–150 nA) reduced the spontaneous firing frequency of nociceptive neurons in the trigeminal nucleus caudalis of decerebrated cats. The response evoked by noxious stimulation (tooth pulp) was gradually inhibited during the 1st minute of application of the opioid and generally remained depressed for 5 min after the current was turned off. These effects of enkephalin were blocked by intravenously or iontophoretically administered naloxone. Nonnociceptive neurons or nociceptive neurons responding to nonnoxious inputs were less frequently inhibited by enkephalin. When tested on nonnociceptive cells, similar applications of substance P usually had little effect. Nociceptive neurons, however, were strongly excited by substance P. This action was not constant and was interrupted by periods of inactivation. Both types of peptide action were similar in temporal aspects. The results suggest a functional interrelationship between enkephalin and substance P in a trigeminal system mediating nociception.

scholarly journals Bilateral Descending Hypothalamic Projections to the Spinal Trigeminal Nucleus Caudalis in Rats

PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e73022 ◽  
Author(s):  
Khaled Abdallah ◽  
Alain Artola ◽  
Lénaic Monconduit ◽  
Radhouane Dallel ◽  
Philippe Luccarini
Keyword(s):  
Spinal Trigeminal Nucleus ◽  
Trigeminal Nucleus ◽  
Trigeminal Nucleus Caudalis ◽  
Spinal Trigeminal Nucleus Caudalis
Sign in / Sign up

Export Citation Format

Share Document