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Axonal regrowth upregulates beta-actin and Jun D mRNA expression

L M Lund1, I G McQuarrie

  • 1VA Medical Center (151 W), Cleveland, Ohio 44106, USA.

Journal of Neurobiology
|December 1, 1996
PubMed

Insights

Axon injury in rats significantly increases beta-actin and Jun D mRNA in spinal cord motor neurons. This suggests axonal regeneration may reactivate developmental programs for neuronal differentiation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Biology

Background:

  • Perturbation of quiescent cells increases expression of genes regulating transcription and cell cycle.
  • Jun and Fos proteins mediate mitogenic signals and influence cell differentiation.
  • Axotomy in neurons increases actin, tubulin, Jun D, and c-Jun proteins, alongside actin mRNA levels.

Purpose of the Study:

  • To investigate if "constitutive" Jun D and beta-actin messages respond to sciatic nerve axotomy.
  • To determine the impact of sciatic nerve injury on specific gene expression in motor neurons.

Main Methods:

  • Sciatic nerve crush in Sprague-Dawley rats.
  • mRNA extraction from spinal cord hemicords.
  • Northern blot analysis for gene expression.
  • In situ hybridization to localize mRNA in motor neurons.
  • Fluoro-Ruby tracing to identify axotomized neurons.

Main Results:

  • A 2.3-fold increase in beta-actin mRNA and a 2.5-fold increase in Jun D mRNA were observed in the lesioned hemicord at 4 days post-axotomy.
  • In situ hybridization confirmed undiminished or increased concentrations of both mRNAs in ipsilateral motor neurons, which had enlarged.
  • Fluoro-Ruby labeling confirmed that only axotomized neurons exhibited enlargement.

Conclusions:

  • Axotomy induces significant increases in beta-actin and Jun D mRNA levels in spinal cord motor neurons.
  • Axonal regeneration shares similarities with the embryonic program for neuronal differentiation.
  • Axotomy reinitiates aspects of the embryonic neuronal differentiation program.

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