ZFIN ID: ZDB-PUB-190405-11
The Neuromodulator Adenosine Regulates Oligodendrocyte Migration at Motor Exit Point Transition Zones
Fontenas, L., Welsh, T.G., Piller, M., Coughenour, P., Gandhi, A.V., Prober, D.A., Kucenas, S.
Date: 2019
Source: Cell Reports   27: 115-128.e5 (Journal)
Registered Authors: Fontenas, Laura, Kucenas, Sarah, Prober, David
Keywords: adenosine, migration, motor exit point glia, motor exit point transition zone, neural activity, oligodendrocyte progenitor cell, zebrafish
MeSH Terms:
  • Adenosine/pharmacology*
  • Animals
  • Animals, Genetically Modified
  • Body Patterning/physiology
  • Cell Differentiation/drug effects
  • Cell Movement/drug effects*
  • Embryo, Nonmammalian
  • Female
  • Male
  • Motor Endplate/cytology
  • Motor Endplate/embryology*
  • Motor Neurons/drug effects
  • Motor Neurons/physiology
  • Neurotransmitter Agents/pharmacology*
  • Oligodendroglia/drug effects*
  • Oligodendroglia/physiology
  • Spinal Cord/cytology
  • Spinal Cord/drug effects
  • Spinal Cord/embryology*
  • Stem Cells/drug effects
  • Stem Cells/physiology
  • Zebrafish/embryology
PubMed: 30943395 Full text @ Cell Rep.
During development, oligodendrocyte progenitor cells (OPCs) migrate extensively throughout the spinal cord. However, their migration is restricted at transition zones (TZs). At these specialized locations, unique glial cells in both zebrafish and mice play a role in preventing peripheral OPC migration, but the mechanisms of this regulation are not understood. To elucidate the mechanisms that mediate OPC segregation at motor exit point (MEP) TZs, we performed an unbiased small-molecule screen. Using chemical screening and in vivo imaging, we discovered that inhibition of A2a adenosine receptors (ARs) causes ectopic OPC migration out of the spinal cord. We provide in vivo evidence that neuromodulation, partially mediated by adenosine, influences OPC migration specifically at the MEP TZ. This work opens exciting possibilities for understanding how OPCs reach their final destinations during development and identifies mechanisms that could promote their migration in disease.