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Systemic administration of insulin‐like growth factor decreases motor neuron cell death and promotes muscle reinnervation
Author(s) -
Vergani Letizia,
Di Giulio Anna Maria,
Losa Matteo,
Rossoni Giuseppe,
Muller Eugenio E.,
Gorio Alfredo
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19981215)54:6<840::aid-jnr12>3.0.co;2-l
Subject(s) - axotomy , reinnervation , denervation , sciatic nerve , motor neuron , endocrinology , medicine , neuromuscular junction , muscle atrophy , atrophy , anatomy , anesthesia , biology , central nervous system , neuroscience , disease
Neonatal sciatic nerve axotomy causes motoneuron death and muscle denervation atrophy. The aim of the present study was to determine whether insulin‐like growth factor‐I (IGF‐I) administration promotes muscle reinnervation and counteracts motor neuron loss after such an injury. Six weeks after sciatic nerve axotomy performed in 2‐day‐old pups, the number of motor neurons, as assessed by retrograde transport of horseradish peroxidase injected into the extensor digitorum longus (EDL) muscle, was reduced from 52 ± 3 to 26 ± 3. Subsequent administration of IGF‐I at the doses of 0.02 mg/kg or 1 mg/kg increased the number of motor neurons to 35 ± 2 and 37 ± 5, respectively. The effect on motoneuron survival was accompanied by improved muscle fibre morphometry and restoration of indirect EDL muscle isometric twitch tension, which was about 80% of control values for both doses of IGF‐I compared with 60% observed with saline treatment. Reinnervated EDL muscle from saline‐treated rats cannot hold tetanic tension, which is, however, achieved after IGF‐I treatment at either dose. Thus, both high and low doses of IGF‐I counteracted motoneuron death and improved muscle reinnervation following neonatal sciatic nerve axotomy. IGF‐I at 5 μg/kg failed to increase muscle reinnervation. J. Neurosci. Res. 54:840–847, 1998. © 1998 Wiley‐Liss, Inc.