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Expression of NMDA receptor mRNAs in rat motoneurons is down-regulated after axotomy

F Piehl1, G Tabar, S Cullheim

  • 1Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.

Insights

Axonal injury in motoneurons causes rapid down-regulation of N-methyl-D-aspartate (NMDA) receptor subunits, regardless of subsequent neuronal death. This suggests heightened excitotoxicity risk early after injury.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Biology

Background:

  • Glutamate excitotoxicity via N-methyl-D-aspartate (NMDA) receptors is implicated in motoneuron death following neonatal axotomy.
  • Understanding NMDA receptor subunit expression changes is crucial for motoneuron survival after injury.

Purpose of the Study:

  • To investigate the expression of NMDA receptor subunits (NR1, NR2B, NR2D mRNA and NR1 protein) in motoneurons after different types of axonal injury.
  • To correlate NMDA receptor expression changes with motoneuron death following injury.

Main Methods:

  • In situ hybridization to detect mRNA expression of NMDA receptor subunits.
  • Immunohistochemistry to assess NR1 subunit protein levels.
  • Comparison of sciatic nerve transection (neonatal and adult) and ventral root avulsion models in rats.

Main Results:

  • All lesion models induced down-regulation of NR1, NR2B, and NR2D mRNA in motoneurons, detectable before significant cell death.
  • Ventral root avulsion, causing the most motoneuron death, showed the strongest mRNA down-regulation.
  • Reduced NR1 mRNA expression was accompanied by decreased NR1 protein levels.

Conclusions:

  • Down-regulation of NMDA receptor subunits is an acute response to axonal injury in motoneurons, irrespective of neuronal death.
  • Lesioned motoneurons exhibit increased susceptibility to excitotoxicity early after injury due to altered NMDA receptor expression.

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