Increase in polyneuronal innervation in frog muscle after muscle injury.

Abstract

SUMMARY1. The proportion of polyneuronal innervation was evaluated electrophysiologically in curare-blocked frog cutaneous pectoris muscles after local injury to the muscle fibres on one side. Focal polyneuronal innervation was revealed by recording end-plate potentials evoked by a gradual increase in the stimulus intensity applied to the motor nerve.2. An increase in the proportion of focally polyneuronally innervated muscle fibres appeared in the injured muscle 3-5 days after injury. The difference between the values obtained 3-5 days and 7-9 days (31 and 38 %, respectively) and the control value (18%) was highly significant. A similar increase in the proportion of pluriinnervated muscle fibres was observed in the contralateral muscle, but after a longer period.3. The different components of complex end-plate potentials (e.p.p.s) usually had similar latencies and rise times in control and experimental muscles. This may indicate that the axons had similar conduction velocities and that synapses were located close to each other. 4. A repeated muscle fibre section 24 h after the initial injury resulted in an enhanced polyneuronal innervation (52 %) 7-9 days after the first section.5. The experiments were repeated on partially blocked muscles in order to detect small e.p.p.s with an amplitude similar to that of spontaneous miniature end-plate potentials (m.e.p.p.s). The proportion of polyneuronally innervated fibres estimated by this technique in control muscles approximated 40 %. Polyneuronal innervation was also found to be significantly increased in cut muscles 7-9 days after muscle injury and a week later in contralateral muscles.6. Combined silver and cholinesterase staining was used to detect morphologically polyneuronal innervation. The comparison of morphological and electrophysiological data indicated that the increase in polyneuronal innervation after muscle injury is likely due to nerve sprouting and formation of new synapses.7. The results suggest that the signal for nerve sprouting originates from the damaged muscle cell and that it is transferred transneuronally to the contralateral side.

Physiologic signaling and viability of the muscle cuff regenerative peripheral nerve interface (MC-RPNI) for intact peripheral nerves

“…This finding is not to be understated, as one could surmise that reinnervation of the muscle cuff could reduce distal axonal count and thereby muscle innervation and function. Based on previous research on peripheral nerve regeneration following partial denervation injuries [73][74][75][76][77][78], we theorize this maintenance of distal muscle function occurs through either collateral axonal sprouting of intact nerve fibers at the level of the MC-RPNI or terminal axonal sprouting of remaining fibers at the distal muscle as a compensatory mechanism. A muscle is able to maintain its function, even with reduced axonal numbers, by having each intact motor unit increase its innervation ratio (the number of muscle fibers innervated by a single motor unit.)…”

“…Proponents of the epineurial window in end-to-side neurorrhaphy often cite that removal of the epineurium creates a localized nerve injury, allowing for generation and diffusion of neurotrophic factors to encourage collateral sprouting [86]. However, this mechanism of axonal sprouting has also been shown to occur independent of the nerve in the setting of muscle injury and denervation through Schwann cell-mediated mechanisms [73][74][75]. In the context of MC-RPNI reinnervation, it is possible that axonal sprouting is primarily mediated by ischemiainduced muscle injury from the harvest of the graft.…”