PUBLICATION

Microglia exit the CNS in spinal root avulsion

Authors
Green, L.A., Nebiolo, J.C., Smith, C.J.
ID
ZDB-PUB-191126-12
Date
2019
Source
PLoS Biology   17: e3000159 (Journal)
Registered Authors
Smith, Cody
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Brachial Plexus/injuries
  • Brachial Plexus/metabolism
  • Cell Communication
  • Cell Movement
  • Embryo, Nonmammalian
  • Gene Expression
  • Genes, Reporter
  • Green Fluorescent Proteins/genetics
  • Green Fluorescent Proteins/metabolism
  • Humans
  • Macrophages/metabolism*
  • Macrophages/pathology
  • Microglia/metabolism*
  • Microglia/pathology
  • Models, Biological
  • Receptors, N-Methyl-D-Aspartate/genetics
  • Receptors, N-Methyl-D-Aspartate/metabolism*
  • Spinal Cord/metabolism
  • Spinal Cord/pathology
  • Spinal Cord Injuries/genetics
  • Spinal Cord Injuries/metabolism*
  • Spinal Cord Injuries/pathology
  • Spinal Nerve Roots/injuries
  • Spinal Nerve Roots/metabolism*
  • Time-Lapse Imaging
  • Zebrafish
PubMed
30794533 Full text @ PLoS Biol.
Abstract
Microglia are central nervous system (CNS)-resident cells. Their ability to migrate outside of the CNS, however, is not understood. Using time-lapse imaging in an obstetrical brachial plexus injury (OBPI) model, we show that microglia squeeze through the spinal boundary and emigrate to peripheral spinal roots. Although both macrophages and microglia respond, microglia are the debris-clearing cell. Once outside the CNS, microglia re-enter the spinal cord in an altered state. These peripheral nervous system (PNS)-experienced microglia can travel to distal CNS areas from the injury site, including the brain, with debris. This emigration is balanced by two mechanisms-induced emigration via N-methyl-D-aspartate receptor (NMDA) dependence and restriction via contact-dependent cellular repulsion with macrophages. These discoveries open the possibility that microglia can migrate outside of their textbook-defined regions in disease states.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping