Despite recent advances in microsurgical techniques and equipments, recovery of function following repair of transected nerves often remains suboptimal. Contrary to traumatic injuries vascular damage that causes peripheral nerve injury has not been well-documented in the literature. In the present study a total of 40 female rats were randomly divided into four groups: Group 1: intact controls (n: 10), Group 2: sham-operated (n: 10), Group 3: vehicle-treated (n: 10), Group 4: melatonin-treated (n: 10). Sciatic nerve damage was created by stripping of the epineurial vessels around the nerve. 50 mg/kg Melatonin was injected intraperitoneally immediately after epineurial stripping in Group 4 in the course of 4 postoperative weeks. We found that melatonin administration after stripping of the epineurial vessels exerted a beneficial effect on axonal regeneration and functional recovery was confirmed by functional (sensory-motor, biochemical, and electrophysiological analyses) and morphological (light microscopic and ultrastructural analyses) data. In the light of these results we concluded that melatonin in a model of sciatic nerve injury leads to axonal regeneration, reducing in oxidative stress, and improved functional recovery.

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BackgroundVincristine-induced peripheral neuropathy (VIPN) is a distal axonopathy characterized by the loss of distal myelinated axons. This study aimed to assess the potential neuroregenerative roles of vitamin D3 using functional and electron microscopic analyses in a rat model of VIPN. MethodologyA total of 40 female Wistar rats were randomly divided into four main groups: Group 1 (control, n = 10), Group 2 (vincristine, n = 10), Group 3 (vincristine + vitamin D3, n = 10), and Group 4 (vincristine + vehicle, n = 10). Vincristine was administered intraperitoneally at a dose of 0.15 mg/kg, for two weeks, to induce peripheral neuropathy. Following successful induction, vitamin D3 (500 IU/kg/day) and vehicle treatments were applied weekly over four weeks. Structural (electron microscopic analysis) and functional analysis (von Frey test, pinch test, and electrophysiological analysis) were performed to assess functional recovery after peripheral nerve impairment. ResultsWithdrawal responses to mechanical allodynia and pinch tests were significantly higher in the vitamin D3treated group (P < 0.05). The electrophysiological analysis also supported these results. Electron microscopic evaluation revealed that the remyelinated nerve fibers in the vitamin D3-treated group (Group 3) had thick myelin sheaths and normal axonal morphology. ConclusionsOur study demonstrated that vitamin D3 could promote functional and structural recovery in a rat model of VIPN. Further studies should be conducted to elucidate the underlying mechanisms by which vitamin D3 exerts its regenerative effects in VIPN, using alternative administration protocols.

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Quantification of consecutive motor unit potential (MUP) is used to diagnose and monitor the progress of neuromuscular pathologies in clinical applications. In this study, a detailed motor unit simulation was conducted to reveal and understand the factors affecting MUPs. Using a volume conductor model and real muscle parameters, normal and pathologic MUPs were created. The shape changes observed in consecutive MUPs, called jiggle, are calculated with a quantification method. Increased jitter duration and re-innervation percentage commonly observed during motor unit loss increase the jiggle value proportionally. Moreover, increasing fiber density changing different regions of a muscle bundle decreases the jiggle value. The blocking phenomena generally observed in re-innervated fibers affects the jiggle value similar to jitter duration. But, higher blocking levels (50%) of re-innervated motor fiber do not have an effect on jiggle value as lower levels of blocking (20%). In conclusion, simulation of pathological MUPs showed that it is useful for clinicians to understand the progress of a neuromuscular pathology and the factors affecting consecutive MUP wave shape.