Spinal microglia contribute to sustained inflammatory pain via amplifying neuronal activity

© 2022. The Author(s)..

Microglia are highly dynamic immune cells of the central nervous system (CNS). Microglial processes interact with neuronal elements constantly on the order of minutes. The functional significance of this acute microglia-neuron interaction and its potential role in the context of pain is still largely unknown. Here, we found that spinal microglia increased their process motility and electrophysiological reactivity within an hour after the insult in a mouse model of formalin-induced acute, sustained, inflammatory pain. Using an ablation strategy to specifically deplete resident microglia in the CNS, we demonstrate that microglia participate in formalin-induced acute sustained pain behaviors by amplifying neuronal activity in the spinal dorsal horn. Moreover, we identified that the P2Y12 receptor, which is specifically expressed in microglia in the CNS, was required for microglial function in formalin-induced pain. Taken together, our study provides a novel insight into the contribution of microglia and the P2Y12 receptor in inflammatory pain that could be used for potential therapeutic strategies.

Medienart:

E-Artikel

Erscheinungsjahr:

2022

Erschienen:

2022

Enthalten in:

Zur Gesamtaufnahme - volume:15

Enthalten in:

Molecular brain - 15(2022), 1 vom: 26. Okt., Seite 86

Sprache:

Englisch

Beteiligte Personen:

Gu, Nan [VerfasserIn]
Yi, Min-Hee [VerfasserIn]
Murugan, Madhuvika [VerfasserIn]
Xie, Manling [VerfasserIn]
Parusel, Sebastian [VerfasserIn]
Peng, Jiyun [VerfasserIn]
Eyo, Ukpong B [VerfasserIn]
Hunt, Christine L [VerfasserIn]
Dong, Hailong [VerfasserIn]
Wu, Long-Jun [VerfasserIn]

Links:

Volltext

Themen:

1HG84L3525
Formaldehyde
Formalin
Inflammatory pain
Journal Article
Microglia
Microglia–neuron interaction
P2Y12 receptor
Purinergic P2Y Receptor Antagonists
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Two-photon imaging

Anmerkungen:

Date Completed 28.10.2022

Date Revised 04.01.2023

published: Electronic

Citation Status MEDLINE

doi:

10.1186/s13041-022-00970-3

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM348039115