CCL2 facilitates spinal synaptic transmission and pain via interaction with presynaptic CCR2 in spinal nociceptor terminals.
Mol Brain
; 13(1): 161, 2020 11 23.
Article
de En
| MEDLINE
| ID: mdl-33228784
ABSTRACT
Previous studies have shown that CCL2 may cause chronic pain, but the exact mechanism of central sensitization is unclear. In this article, we further explore the presynaptic role of CCL2. Behavioral experiments show that intervertebral foramen injection CCR2 antagonists into dorsal root ganglion (DRG) can inhibit the inflammatory pain caused by CCL2 in spinal cord. We raised the question of the role of presynaptic CCR2 in the spinal dorsal horn. Subsequent electron microscopy experiments showed that CCR2 was expressed in the presynaptic CGRP terminal in the spinal dorsal horn. CCL2 can enhance presynaptic calcium signal. Whole-cell patch-clamp recordings showed that CCL2 can enhance NMDAR-eEPSCs through presynaptic effects, and further application of glutamate sensor method proved that CCL2 can act on presynaptic CCR2 to increase the release of presynaptic glutamate. In conclusion, we suggest that CCL2 can directly act on the CCR2 on presynaptic terminals of sensory neurons in the spinal dorsal horn, leading to an increase in the release of presynaptic glutamate and participate in the formation of central sensitization.
Mots clés
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Douleur
/
Moelle spinale
/
Nocicepteurs
/
Terminaisons présynaptiques
/
Transmission synaptique
/
Chimiokine CCL2
/
Récepteurs CCR2
Limites:
Animals
Langue:
En
Journal:
Mol Brain
Sujet du journal:
BIOLOGIA MOLECULAR
/
CEREBRO
Année:
2020
Type de document:
Article
Pays d'affiliation:
Chine