Peripheral nerve injury

Clarke, David B.; Richardson, P. M.

doi:10.1097/00019052-199410000-00009

Cited by 45 publications

(28 citation statements)

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“…First, there is not an excessive release of excitatory amino acids leading to hyperactivity of nNOS. Second, in contrast to cerebral ischemia, in which inflammatory cells contribute to the tissue damage Chopp et al, 1994), the presence of Schwann cells and macrophages provides support for removing debris and releasing growth factors and adhesion molecules required in regeneration (Perry and Brown, 1992a,b;Griffin and Hoffman, 1993;Clarke and Richardson, 1994). Third, each NOS isoform becomes positive 2 days after lesion at different places: nNOS in DRG neurons and axons of the proximal stump, eNOS in vessels of the distal segment, and iNOS in recruited macrophages of the external perineurium.…”

Section: Comparison With Cerebral Ischemia (A Process Where the Threementioning

confidence: 99%

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Expression of three forms of nitric oxide synthase in peripheral nerve regeneration

González‐Hernández

Rustioni

1999

J. Neurosci. Res.

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Nitric oxide (NO) is a short-lived molecule with messenger and cytotoxic functions in nervous, cardiovascular, and immune systems. Nitric oxide synthase (NOS), the enzyme responsible for NO synthesis, exists in three different forms: the neuronal (nNOS), present in discrete neuronal populations; the endothelial (eNOS), present in vascular endotheliun, and the inducible isoform (iNOS), expressed in various cell types when activated, including macrophages and glial cells. In this study, we have investigated the possible involvement of NO in Wallerian degeneration and the subsequent regeneration occurring after sciatic nerve ligature, using histochemistry and immunocytochemistry for the three NOS isoforms, at different postinjury periods. Two days after lesion, the three NOS isoforms are overexpressed, reaching their greatest expression during the second week. nNOS is upregulated in dorsal root ganglion neurons, centrifugally transported and accumulated in growing axons. eNOS is overexpressed in vasa nervorum of the distal stump and around ligature, and iNOS is induced in recruited macrophages. These findings indicate that different cellular sources contribute to maintain high levels of NO at the lesion site. The parallelism between NOS inductions and well-known repair phenomena suggests that NO, acting in different ways, may exert a beneficial effect on nerve regeneration.

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Section: Comparison With Cerebral Ischemia (A Process Where the Threementioning

confidence: 99%

“…At present, we know that macrophages play an essential role in the healing process, turning degenerating nerve into the appropriate environment for a successful axonal regrowth (Perry and Brown, 1992a,b;Friede and Brück, 1993;Clarke and Richardson, 1994). Resident macrophages are sparse in normal peripheral nerves.…”

Section: Inosmentioning

confidence: 99%

Expression of three forms of nitric oxide synthase in peripheral nerve regeneration

González‐Hernández

Rustioni

1999

J. Neurosci. Res.

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“…If a Schwann cell in the distal segment of a transected nerve is not contacted by a regenerating sprout within 6 months, it will start to lose its axon binding and guiding capability. 3 There-fore, once the eventual functional recovery proves to be poor this leaves only a short period of time to correct the nerve reconstruction while leaving sufficient time for the sprouts to again regenerate into the distal segment.…”

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confidence: 99%

A magnetic evaluation of peripheral nerve regeneration: II. The signal amplitude in the distal segment in relation to functional recovery

et al. 1998

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“…Therefore, we thought that a decrease in oxidative stress due to selenium may have a positive effect on Schwann cells. Reactive oxygen species and nitric oxide were increased after trauma in a peripheral nerve exposed to trauma, and Schwann cells, which play an influential role in the release of neurotrophic factors in peripheral nerve healing, could induce apoptosis via the mitochondrial pathway, depending on the dose and duration of oxidative stress (33)(34)(35)(36)(37)(38)(39). There are some limitations of this study.…”

Section: Discussionmentioning

confidence: 99%

Effects of Selenium on Axon and Myelin Healing in an Experimental Sciatic Nerve Injury Model

Kızılay¹,

Erken²,

Aktaş³

et al. 2017

İstanbul Tıp Fakültesi Dergisi

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Objective: Although, the neuroprotective effects of selenium are known, its effect on peripheral nerve injury is not clear. The study was aimed to investigate whether selenium prevents axonal and myelin damage in experimental sciatic nerve injury. Materials and Methods: Twenty-eight male Wistar albino rats were divided into four groups (n=7 in each): control (C), selenium (S), injury (I), and selenium-treated injury (SI). Injury was generated by 30 second of compression via Yasargil aneurysm clip on the sciatic nerve of rats in the I and SI groups. Then, selenium was given to the S and SI groups as 1.5 mg/ kg by oral gavage at 1 st , 24 th , 48 th and 72 nd hour after surgery. According to the experimental protocol, electrophysiological, histological, and biochemical tests were performed end of the day 4. Results: Whereas the amplitude of compound action potential, nerve conduction velocity, average axon diameter, myelin thickness, myelinated/unmyelinated axons and SOD activity in red blood cells of the I group were significantly lower than those of the C, S and SI groups, the serum MDA levels of the I group were significantly higher than those of the C, S and SI groups. Conclusion:The findings of this study show that selenium decreases axonal and myelin damage after sciatic nerve injury and that this neuroprotective effect of selenium is at least partially mediated by oxidant/antioxidant mechanisms.

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Peripheral nerve injury

Cited by 45 publications

References 0 publications

Expression of three forms of nitric oxide synthase in peripheral nerve regeneration

Expression of three forms of nitric oxide synthase in peripheral nerve regeneration

A magnetic evaluation of peripheral nerve regeneration: II. The signal amplitude in the distal segment in relation to functional recovery

Effects of Selenium on Axon and Myelin Healing in an Experimental Sciatic Nerve Injury Model

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