Related Experiment Video
Updated: Feb 28, 2026
10:52
Chronic Constriction Injury of the Rat's Infraorbital Nerve IoN-CCI to Study Trigeminal Neuropathic Pain
Published on: September 21, 2015
20.9K
Neuron-glia interaction is a key mechanism underlying persistent orofacial pain
Koichi Iwata1, Ayano Katagiri1, Masamichi Shinoda1
1Department of Physiology, Nihon University School of Dentistry.
Journal of Oral Science
|June 23, 2017
Summary
Following orofacial inflammation or nerve injury, trigeminal neurons become hyperexcitable. This neuronal hyperexcitability, involving glial cells, drives persistent orofacial pain.
Area of Science:
- Neuroscience
- Pain Research
- Glial Cell Biology
Background:
- Orofacial inflammation and trigeminal nerve injury enhance neuronal excitability in the trigeminal ganglion (TG), trigeminal spinal subnucleus caudalis (Vc), and upper cervical spinal cord (C1-C2).
- Sensitized neurons release molecules that modulate excitability, contributing to long-lasting sensitization.
Purpose of the Study:
- To investigate the role of neuronal-glial interactions in persistent orofacial pain.
- To understand the molecular mechanisms underlying trigeminal sensitization and pain.
Main Methods:
- The study focused on analyzing the excitability changes in TG, Vc, and C1-C2 neurons.
- Investigated the activation of satellite glial cells (TG) and microglia/astrocytes (Vc, C1-C2) in response to neuronal hyperexcitability.
- Examined the molecular signaling between neurons and glial cells in the trigeminal pain pathway.
Main Results:
- Hyperexcitable nociceptive neurons activate glial cells throughout the TG, Vc, and C1-C2.
- Activated glial cells release molecules that further modulate nociceptive neuron activity.
- A widespread glial activation pattern emerges, contributing to the spread and maintenance of sensitization.
Conclusions:
- Functional interactions between neurons and glial cells are crucial for persistent orofacial pain.
- Glial cell activation is a key component in the pathophysiology of orofacial inflammation and trigeminal nerve injury-induced pain.
- Targeting neuronal-glial communication may offer therapeutic strategies for chronic orofacial pain.
More Related Videos
05:38Author Spotlight: Utilizing Infraorbital Nerve Ligation in Mice for Investigating Trigeminal Neuropathic Pain and Treatment Strategies
Published on: March 8, 2024
3.0K
07:39Assessment of Nerve Injury-Induced Mechanical Hypersensitivity in Rats Using an Orofacial Operant Pain Assay
Published on: July 26, 2022
4.3K
Related Concept Videos
01:44Nociception
33.5K
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.
33.5K
01:03Olfactory Receptors: Location and Structure
12.3K
The process of olfaction, also known as the sense of smell, is a sophisticated chemical response system. The specialized sensory neurons that facilitate this process, known as olfactory receptor neurons, are situated in an upper segment of the nasal cavity, known as the olfactory epithelium. Olfactory sensory neurons are bipolar, with their dendrites extending from the epithelium's apex into the mucus that lines the nasal cavity. Airborne molecules, when inhaled, traverse the olfactory...
12.3K
01:25Analgesia and Pain Management
2.4K
Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...
2.4K
01:20Pain
1.6K
Pain serves as a critical warning signal that alerts the body to potential or actual harm. When mechanical pressure on the skin is intense, such as from a sharp pinch, the sensation transitions from touch to pain. Similarly, extreme temperatures, like a hot pot handle, convert the sensation of heat into pain. Pain can also result from overstimulation of other senses, such as blinding light, loud noise, or the intense heat from habañero peppers. This ability to sense pain is essential for...
1.6K
01:30Ligand-Gated Ion Channel Receptor: Gating Mechanism
4.4K
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...
4.4K
01:15Neurogenesis and Regeneration of Nervous Tissue
1.8K
In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
1.8K