The Role of Microglia in Neuroinflammation of the Spinal Cord after Peripheral Nerve Injury.

axotomy microglia motoneurons neuroinflammation neuroprotection regeneration sensory neurons synaptic plasticity

Journal

Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052

Informations de publication

Date de publication:
30 06 2022
Historique:
received: 03 06 2022
revised: 26 06 2022
accepted: 27 06 2022
entrez: 9 7 2022
pubmed: 10 7 2022
medline: 14 7 2022
Statut: epublish

Résumé

Peripheral nerve injuries induce a pronounced immune reaction within the spinal cord, largely governed by microglia activation in both the dorsal and ventral horns. The mechanisms of activation and response of microglia are diverse depending on the location within the spinal cord, type, severity, and proximity of injury, as well as the age and species of the organism. Thanks to recent advancements in neuro-immune research techniques, such as single-cell transcriptomics, novel genetic mouse models, and live imaging, a vast amount of literature has come to light regarding the mechanisms of microglial activation and alluding to the function of microgliosis around injured motoneurons and sensory afferents. Herein, we provide a comparative analysis of the dorsal and ventral horns in relation to mechanisms of microglia activation (CSF1, DAP12, CCR2, Fractalkine signaling, Toll-like receptors, and purinergic signaling), and functionality in neuroprotection, degeneration, regeneration, synaptic plasticity, and spinal circuit reorganization following peripheral nerve injury. This review aims to shed new light on unsettled controversies regarding the diversity of spinal microglial-neuronal interactions following injury.

Identifiants

pubmed: 35805167
pii: cells11132083
doi: 10.3390/cells11132083
pmc: PMC9265514
pii:
doi:

Types de publication

Journal Article Review Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NINDS NIH HHS
ID : F32 NS112556
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS111969
Pays : United States
Organisme : NINDS NIH HHS
ID : T32 NS096050
Pays : United States

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Auteurs

Tana S Pottorf (TS)

Department of Cell Biology, Emory University, Atlanta, GA 30322, USA.

Travis M Rotterman (TM)

School of Biological Sciences, Georgia Institute of Technology, Atlanta, GA 30318, USA.

William M McCallum (WM)

Department of Cell Biology, Emory University, Atlanta, GA 30322, USA.

Zoë A Haley-Johnson (ZA)

Department of Cell Biology, Emory University, Atlanta, GA 30322, USA.

Francisco J Alvarez (FJ)

Department of Cell Biology, Emory University, Atlanta, GA 30322, USA.

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