Different pattern of recovery of fast and slow muscles following nerve injury in the rat.

Abstract

SUMMARY1. The sciatic nerve was crushed in 5-6-day-old rats and the time course of recovery and changes in physiological and morphological properties of reinnervated fast and slow muscles was compared.2. The maximal tetanic tension developed by the reinnervated muscles was recorded at different times from about 18 days of age, when functional recovery was first seen, until 2 months.3. The maximal indirectly elicited tetanic tension of the reinnervated slow soleus muscle gradually increased from 55 % of normal at 18 days to 75 % of normal at 2 months. In contrast, the tension of the reinnervated fast muscle extensor digitorum longus (e.d.l.) fell sharply from 70 % of normal at 18 days to 40 % at 21 days and remained at that level till the end of the study. 4. The total number of muscle fibres in control, reinnervated and denervated e.d.l. muscles was counted. At 18 days the number of fibres in the reinnervated e.d.l. was similar to normal but by 1 month it had fallen to one-third. This decrease did not take place in permanently denervated muscles until at least 35 days. Loss of fibres in the reinnervated soleus was small.5. During the early stages of reinnervation the contraction and relaxation of the fast muscles was very prolonged. By 1 month the time taken to reach peak twitch tension had decreased to normal values but the relaxation was still slower and remained so for several months.6. The study of fatigue resistance showed that at 18 days the reinnervated fast muscles were as fatigable as normal muscles from animals of the same age. The fatigability of normal muscles increased with age to adult levels, but the reinnervated muscles became more fatigue resistant and remained so.7. Our findings suggest that fast muscles become selectively impaired after nerve injury at 6 days because they lose a large number of fibres after reinnervation.

Effects of age and nerve-repair grafts on reinnervation and fiber type distribution of rat medial gastrocnemius muscles

“…Previous studies have demonstrated that the process of reinnervation by Type I fibers is faster than by Type IIB fibers (Lowrie and Vrbova, 1984;Choi et al, 1996). In accordance, preferential reinnervation of Type I fibers following nerve-repair leads to an increase in typegrouping of Type I fibers in reinnervated muscle (Karpati and Engel, 1968;Albani et al, 1988;Yoshimura et al, 1999).…”

Over-expression of parvalbumin in transgenic mice rescues motoneurons from injury-induced cell death

“…Even in the adult, where there is no loss of motoneurons following nerve injury (Vanden Noven et al, 1993), prolonged denervation can result in incomplete recovery of muscle function (Gordon and Fu, 1997), although the shorter the period of denervation, the more complete the recovery of the muscle. Following neonatal nerve injury, which results in extensive motoneuron death, muscles never fully recover even after reinnervation (Lowrie et al, 1982(Lowrie et al, , 1987Lowrie and Vrbová, 1984;Albani et al, 1988;Murali et al, 1996). After neonatal nerve crush in rats, regenerating axons reach the muscles earlier than in the adult (Murali et al, 1996).…”

“…Despite this, reinnervated fast muscles become weaker due to the loss of muscle fibers and a proportion of the endplates disintegrate. Fast muscles become more fatigue resistant (Lowrie et al, 1982(Lowrie et al, , 1987Lowrie and Vrbová, 1984) and the organisation of the motor unit is altered (Albani et al, 1988), although this may be largely due to the loss of motoneurons. It has been suggested that following nerve injury, the period for which the muscle is isolated from the motoneuron, retards the differentiation of the muscle (Lowrie and Vrbová, 1984).…”

Characterization of Neuronal Death and Functional Deficits following Nerve Injury during the Early Postnatal Developmental Period in Rats

“…Contrary to adult rodent nerve injury models where limited to no cell death occurs, crushing of neonatal sciatic nerves prior to postnatal day 5 (P5) leads to substantial neuronal death, resulting in severe functional impairments [17][18][19][20] . Although glutamate-mediated cell death has been implicated in the underlying pathology, neuronal death has also been shown to result from the inability of immature Schwann cells (SCs) to maintain a proregenerative environment in the distal stump of the nerve [15] .…”

“…The majority of nerve crush injuries in adult rodent models are performed at the mid-thigh level. For this reason, in this study we used a mid-thigh nerve crush in the neonate, which is a much more proximal nerve injury than reported in previous studies [13,17,23,25] .…”