Skeletal muscle structure and function are dependent on intact innervation. Prolonged muscle denervation results in irreversible muscle fiber atrophy, connective tissue hyperplasia, and deterioration of muscle spindles, specialized sensory receptors necessary for proper skeletal muscle function. The protective effect of temporary sensory innervation on denervated muscle, before motor nerve repair, has been shown in the rat. Sensory-protected muscles exhibit less fiber atrophy and connective tissue hyperplasia and maintain greater functional capacity than denervated muscles. The purpose of this study was to determine whether temporary sensory innervation also protects muscle spindles from degeneration.
Rat tibial nerve was transected and repaired with either the saphenous or the original transected nerve. Negative controls remained denervated. After 3 to 6 months, the electrophysiologic response of the nerve to stretch in the rat gastrocnemius muscle was measured (n = 3 per group). After the animals were euthanized, the gastrocnemius muscle was removed, sectioned, stained, and examined for spindle number (n = 3 per group) and morphology (one rat per group). Immunohistochemical assessment of muscle spindle innervation was examined in four additional animals.
Significant deterioration of muscle spindles was seen in denervated muscle, whereas in muscle reinnervated with the tibial or the saphenous nerve, spindle number and morphology were improved. Histologic and functional evidence of spindle reinnervation by the sensory nerve was obtained.
These findings add to the known means by which motor or sensory nerves exert protective effects on denervated muscle, and further promote the use of sensory protection for improving the outcome after peripheral nerve injury.
Hamilton, Ontario, Canada
From the Department of Psychiatry and Behavioral Neurosciences, the Department of Pathology and Molecular Medicine, and the Division of Plastic Surgery, Department of Surgery, McMaster University.
Received for publication January 20, 2008; accepted June 15, 2009.
Presented at the 16th Annual Scientific Meeting of the American Society for Peripheral Nerve, in Beverly Hills, California, January 11 through 13, 2008.
Disclosure: None of the authors has a financial interest in any of the products, devices, or drugs mentioned in this article.
Margaret Fahnestock, Ph.D. Department of Psychiatry and Behavioral Neurosciences; McMaster University; 1200 Main Street West; Hamilton, Ontario L8N 3Z5, Canada; firstname.lastname@example.org