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Plasminogen activators in the neuromuscular system of the wobbler mutant mouse

B Blondet1, G Barlovatz-Meimon, B W Festoff

  • 1INSERM U. 153, CNRS URA 614, Paris, France.

Brain Research
|May 15, 1992
PubMed

Insights

In wobbler mice, a model for lower motoneuron disorders, increased muscle plasminogen activator (PA) activity, particularly urokinase-type PA (uPA), correlates with denervation and reinnervation. This contrasts with normal development and experimental denervation, highlighting uPA

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • The wobbler mouse model exhibits lower motoneuron degeneration, muscle atrophy, denervation, and reinnervation.
  • Plasminogen activator (PA) activity typically decreases during normal neuromuscular synapse maturation.
  • Experimental denervation in adult mice increases muscle PA activity.

Purpose of the Study:

  • To investigate the role of PAs in the denervation/reinnervation processes and motoneuron degeneration observed in wobbler mice.
  • To assess PA involvement in the specific pathological changes characteristic of the wobbler mutation.

Main Methods:

  • Choline acetyltransferase (ChAT) activity was measured in spinal cord and muscle (biceps brachii, gastrocnemius) to assess innervation.
  • Motoneuron terminal sprouting was evaluated using silver/cholinesterase staining.
  • Specific PA activities in muscle and spinal cord extracts were determined using amidolytic assays and fibrin zymography.

Main Results:

  • Wobbler mice showed significantly decreased ChAT activity in biceps brachii and gastrocnemius muscles, but not in spinal cord.
  • Motoneuron terminal sprouting was observed in 40% of neuromuscular junctions in wobbler mice.
  • Increased PA activity, predominantly urokinase-type PA (uPA), was found in wobbler mouse muscles, with higher levels in the more affected biceps brachii.

Conclusions:

  • Plasminogen activators, especially uPA, are implicated in the denervation and reinnervation phenomena of the wobbler mouse model.
  • The differential increase in uPA activity between muscles correlates with the varying severity of impairment caused by the wobbler mutation.
  • These findings suggest a specific role for muscle-derived uPA in the pathophysiology of this lower motoneuron disorder.

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