Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Nociception01:44

Nociception

32.6K
Nociception—the ability to feel pain—is essential for an organism’s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain.
32.6K
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

3.5K
Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
3.5K
GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

6.7K
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
6.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

A prospective cohort study comparing the effects of different middle turbinate treatments on olfactory function recovery in CRSwNP patients after FESS.

Rhinology·2025
Same author

[Applications and challenges of behavioral economics theory in HIV/AIDS response].

Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]·2025
Same author

Modified 'cross-stealing' repair of nasal septal perforation using unilateral inverted mucosal flap.

European annals of otorhinolaryngology, head and neck diseases·2025
Same author

[Epidemic characteristics of HIV-infected people among Chinese and Burmese in Dehong Dai and Jingpo Autonomous Prefecture of Yunnan Province, 2000-2023].

Zhonghua liu xing bing xue za zhi = Zhonghua liuxingbingxue zazhi·2024
Same author

Predictive model for postoperative unrecovered olfactory function in CRSwNP patients with olfactory disorder.

Rhinology·2024
Same author

[Calcification distributional density of the aortic-valvular complex is an independent risk factor for conduction block following self-expanding transcatheter aortic valve replacement].

Nan fang yi ke da xue xue bao = Journal of Southern Medical University·2023

Related Experiment Video

Updated: Dec 10, 2025

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents
08:39

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents

Published on: May 16, 2022

2.8K

CGRP Modulates Orofacial Pain through Mediating Neuron-Glia Crosstalk.

H Liang1,2, H Hu1, D Shan1

  • 1State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

Journal of Dental Research
|August 28, 2020
PubMed
Summary

Calcitonin gene-related peptide (CGRP) drives orofacial pain by enhancing nitric oxide production in glial cells, which then stimulates more CGRP release from neurons, creating a pain-amplifying feedback loop.

Keywords:
RNA interferencecalcium channelslentivirusnitric oxidesatellite glial cellstrigeminal ganglia

More Related Videos

Chronic Constriction Injury of the Rat's Infraorbital Nerve IoN-CCI to Study Trigeminal Neuropathic Pain
10:52

Chronic Constriction Injury of the Rat's Infraorbital Nerve IoN-CCI to Study Trigeminal Neuropathic Pain

Published on: September 21, 2015

20.4K
Cell Subtype-specific Analysis of Neuronal Membrane Proteasome in Somatosensory Neurons
09:27

Cell Subtype-specific Analysis of Neuronal Membrane Proteasome in Somatosensory Neurons

Published on: October 10, 2025

333

Related Experiment Videos

Last Updated: Dec 10, 2025

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents
08:39

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents

Published on: May 16, 2022

2.8K
Chronic Constriction Injury of the Rat's Infraorbital Nerve IoN-CCI to Study Trigeminal Neuropathic Pain
10:52

Chronic Constriction Injury of the Rat's Infraorbital Nerve IoN-CCI to Study Trigeminal Neuropathic Pain

Published on: September 21, 2015

20.4K
Cell Subtype-specific Analysis of Neuronal Membrane Proteasome in Somatosensory Neurons
09:27

Cell Subtype-specific Analysis of Neuronal Membrane Proteasome in Somatosensory Neurons

Published on: October 10, 2025

333

Area of Science:

  • Neuroscience
  • Pain Research
  • Cellular Biology

Background:

  • Calcitonin gene-related peptide (CGRP) is implicated in orofacial pain modulation.
  • Neuron-glia interactions are increasingly recognized in pain signaling pathways.

Purpose of the Study:

  • To investigate the mechanisms of CGRP-mediated neuron-glia crosstalk in orofacial pain.
  • To elucidate the role of CGRP and nitric oxide in trigeminal pain signaling.

Main Methods:

  • Orofacial pain model induced by ligating closed-coil springs.
  • Primary culture of trigeminal neurons and satellite glial cells (SGCs).
  • Analysis of gene and protein expression (immunostaining, PCR, Western blot).
  • Assessment of orofacial pain using the rat grimace scale.

Main Results:

  • CGRP expression increased in trigeminal neurons and SGCs during orofacial pain.
  • CGRP administration exacerbated pain; olcegepant alleviated pain.
  • CGRP knockdown reduced CGRP levels and alleviated pain.
  • CGRP upregulated inducible nitric oxide synthase (iNOS) in SGCs via the p38 pathway.
  • Nitric oxide donor (L-arginine) enhanced pain by increasing CGRP expression.
  • L-arginine increased CGRP expression in neurons via N-type calcium channels.

Conclusions:

  • CGRP modulates orofacial pain by upregulating nitric oxide production in SGCs.
  • Nitric oxide stimulates CGRP expression in neurons through N-type calcium channels.
  • This establishes a positive-feedback loop of CGRP-mediated neuron-glia crosstalk in orofacial pain.