Differential recovery of neuromuscular function after nerve/muscle injury induced by crude venom from Notechis scutatus, cardiotoxin from Naja atra and bupivacaine treatments in mice

• Published in: Neuroscience research Vol. 58; no. 3; pp. 317 - 323
• Main Authors: Vignaud, A., Hourdé, C., Butler-Browne, G., Ferry, A.
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier Ireland Ltd 01-07-2007
• Subjects: Anaesthetic; Analysis of Variance; Animals; Bupivacaine; Cobra Cardiotoxin Proteins; Elapid Venoms; Injury; Male; Mice; Muscle; Muscular Diseases - chemically induced; Muscular Diseases - physiopathology; Neuromuscular Junction - physiopathology; Peripheral Nervous System Diseases - chemically induced; Peripheral Nervous System Diseases - physiopathology; Recovery of Function - physiology; Regeneration; Snake venom; Time Factors; Toxinl; Regeneration; Toxinl; Snake venom; Muscle; Anaesthetic; Injury
• ISSN: 0168-0102; 1872-8111
• DOI: 10.1016/j.neures.2007.04.001

Different neuromyotoxic agents are frequently used in rodent models of skeletal nerve/muscle injury and repair. However, their differential effects are not well known. Right
Tibialis anterior muscles of mice were injured by one of three different neuromyotoxic agents: crude venom from
Notechis scutatus, cardiotoxin from
Naja atra or bupivacaine (local anesthetic). Mice were studied 5, 14 and 56 days after injury by analysing the recovery of
in situ muscle isometric function in response to nerve stimulation, muscle weights and muscle histology. Our results show that at day 5 venom treatment had a more debilitating effect on muscle weights and maximal tetanic force than cardiotoxin and bupivacaine treatments (
p
<
0.05). Moreover, the degree of recovery of muscle parameters 14 days after neuromyotoxic treatment varies as follow: venom
<
bupivacaine
<
cardiotoxin. By day 56, we found that injured muscles still exhibit deficits in maximal tetanic force (cardiotoxin and bupivacaine treatments) and fatigue resistance (venom and cardiotoxin treatments) as compared to control muscles (
p
<
0.05). In conclusion, these results indicate that neuromyotoxic agents induce differential destructive effects and recovery in mice and confirm the fact that full nerve/muscle repair is slow and in some cases may never be attained.