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At least 19 recordsLinked to original sources
PubMed1993

Blood-nerve barrier: ultrastructural and endothelial surface charge alterations following nerve crush.

Nerve crush results in an enhanced vascular permeability of the endoneurial vessels distal to the lesion. Vascular permeability at the blood-nerve barrier (BNB) to serum proteins is influenced by many factors, including anionic surface charge, endothelial vesicular transcytosis and the presence or absence of fenestrated vessels. Using mice and rats, the present ultrastructural investigation examined the effect of nerve crush (axonotmesis) on: (1) the distribution of endothelial anionic sites and (2) the appearance of fenestrations in endoneurial vessels after 4 and 14 day intervals as demonstrated with cationic probes. Transient anionic fenestrations developed in a minority of mouse endoneurial vessels in 4-day crushed nerves, but were not found in 14-day crushed nerves of mice nor in crushed nerves of rats. The known increase in the permeability of endoneurial vessels in rats and mice was not associated with reduced luminal labelling with cationic ferritin at physiological pH. At pH 2.0 the labelling of glycocalyx moieties (such as sialic acid) with cationic colloidal gold was disrupted in some epi- and endoneurial vessels of 4-day rats, but in a greater proportion after 14 days. The enhanced permeability of the BNB during degeneration and regeneration is related to the formation of anionic fenestrations in endoneurial vessels of mice and to the reduced and uneven distribution of endothelial glycocalyx moieties that are anionic at pH 2.0 in rats.

Animals↗
PubMed2004

The recovery of blood-nerve barrier in crush nerve injury--a quantitative analysis utilizing immunohistochemistry.

The purpose of this study is to reveal whether the application of immunohistochemical examinations to the peripheral nervous system (PNS) can be a reliable method for the quantitative analysis of the blood-nerve barrier (BNB) and the relationship between restoration of BNB and nerve regeneration. Sciatic nerves in rats were examined after nerve crush. Immunohistochemical staining with anti-rat endothelial cell antigen-1 (anti-RECA-1) that recognizes endothelial cells and anti-endothelial barrier antigen (anti-EBA) for the detection of barrier-type endothelial cells were used. Neurofilament for staining axons was also performed. A quantitative analysis of the BNB was assessed using the ratio of EBA positive cells and RECA-1 positive cells. The ratio of EBA/RECA-1 decreased significantly 3 days postoperatively and reached its lowest level at day 7 in the segment 5 mm proximal and the entire distal stump. The ratio gradually recovered from the proximal and the regeneration of axons started a week earlier than BNB. The ratio of EBA/RECA-1 applied to the PNS can be a reliable method for the quantitative analysis of BNB. In crush injuries, the breakdown of BNB occurred simultaneously in the segment 5 mm proximal and the entire distal stump; restoration began from the proximal to distal and followed a week later to nerve regeneration.

Animals↗
PubMed2001

Induction of the plasminogen activator system accompanies peripheral nerve regeneration after sciatic nerve crush.

Peripheral nerve regeneration is dependent on the ability of regenerating neurites to migrate through cellular debris and altered extracellular matrix at the injury site, grow along the residual distal nerve sheath conduit, and reinnervate synaptic targets. In cell culture, growth cones of regenerating axons secrete proteases, specifically plasminogen activators (PAs), which are believed to facilitate growth cone movement by digesting extracellular matrices and cell adhesions. In this study, the PA system was shown to be specifically activated in sensory neurons after sciatic nerve crush in adult mice. The number of sensory neurons expressing urokinase PA receptor (uPAR) mRNA levels increased above sham levels by 8 hr after crush, whereas the number of sensory neurons expressing uPA and tissue PA (tPA) mRNAs was significantly increased by 3 d after crush. PA mRNA levels were also increased at the crush site, with uPA mRNA elevated by 8 hr after crush and tPA and uPAR mRNA levels markedly increased by 7 d. PA-dependent enzymatic activity was significantly increased from 1 to 7 d after crush in nerves that had been crushed compared with uncrushed nerves. Immunohistochemistry showed that tPA was localized within regenerating axons of the sciatic nerve. There were no significant changes in plasminogen activator inhibitor 1 activity between crush and sham after the injury. These results clearly demonstrated that after injury the PA system was rapidly induced in sensory neurons, where it may play an important role in nerve regeneration in vivo.

Animals↗
PubMed1994

Neuromuscular regeneration by buccal motoneuron B15 after peripheral nerve crush in Aplysia californica.

1. We studied regeneration of neuromuscular connections by identified buccal motoneuron B15 after axotomy produced by crushing nerve 4; the intact contralateral nerve 4 served as control. Electrophysiological recordings, intracellular dye injections, and light and electron microscopy were used to characterize the nature and time course of neuromuscular reinnervation as well as the fate of the isolated distal stump of the motor axon. 2. Axonal outgrowth or sprouting in the form of numerous "regenerites" occurred from the proximal stump of the transected B15 axon, and these regenerites projected through the crush site along the length of the nerve to innervate target muscles at the periphery. 3. Reinnervation of one of the target muscles, the accessory radula closer (I5), was first detected 3 wk after nerve crush. Neuromuscular excitatory postsynaptic potentials measured in individual I5 muscle fibers were initially small and approached control amplitudes by 8 wk postlesion. Newly regenerated neuromuscular synapses displayed facilitation and depression to repeated B15 stimulation with properties similar to those of control synapses, even at early times postlesion. 4. Reinnervation of other buccal muscles by B15, such as I4, appeared slightly delayed relative to that observed for I5. No evidence of abnormal or enlarged fields of innervation were observed, and as in control preparations, regenerated neuromuscular connections were strictly limited to muscles ipsilateral to the B15 cell body. 5. Physiological evidence suggested that the distal axon stumps of B15, although isolated from their cell bodies, survive for several weeks after axotomy. In addition, several large axon profiles indicative of motor axons were seen in cross-sections of nerve 4 taken close to the muscle and distal to the crush site, indicating survival of distal axon stumps. 6. When B15 was selectively stimulated, the newly formed regenerites failed to fire the distal axon stump of B15, demonstrating that the regenerites do not reinnervate the distal stump. 7. Degeneration of axons in nerve 4 distal to the crush site was observed in cross-sections of the nerve at 8 wk postlesion; using ultrathin sections we found cellular debris in individual axon profiles as well as large acellular masses within nerve 4, the latter likely representing the concretion of many axons. Additional evidence for such degenerative changes appeared in the form of autofluorescing spherical bodies or "spheroids" both in individual axons and the nerve distal to the crush site.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

Traumatic brain injury induced neuroprotection of retinal ganglion cells to optic nerve crush.

Optic nerve crush injury leads to death of retinal ganglion cells (RGCs), both as a direct result of the primary injury and via secondary degeneration induced by neurotoxins secreted by dying RGCs. Studies have shown that, if optic nerve crush is preceded by an unrelated injury to another part of the central nervous system, for example, the spinal cord, the ensuing T cell-mediated protective autoimmunity results in a significant increase in RGC survival. In this study, we used the controlled cortical impact paradigm to induce unilateral traumatic brain injury (TBI) in rats at different times before they were contralaterally subjected to a mild optic nerve crush. Survival of RGCs, assessed 2 weeks after crush injury, was significantly increased when the crush was inflicted 11 days after TBI, but not when the two injuries were concomitant. The beneficial effect was unaffected by injection of low-dose methylprednisolone MP (1 mg/kg), but was inhibited after a high-dose injection (30 mg/kg). Brain-derived neurotrophic factor (BDNF) mRNA, assayed at intervals after TBI, was increased in the retina ipsilateral to TBI but decreased in the contralateral retina. BDNF peaked 1 day after TBI, decreased on day 11, and rose again on day 21. It thus seems that brain injury sustained a certain time before optic nerve injury has a protective effect on RGC survival. This neuroprotective effect, which appears unrelated to retinal BDNF, is inhibited by high-dose MP, commonly used clinically to treat traumatic optic neuropathy.

Animals↗
PubMed2005

Spatiotemporal quantification of recruit and resident macrophages after crush nerve injury utilizing immunohistochemistry.

The purpose of this study was to investigate quantitatively the temporal and spatial regulation and the morphological changes of the recruit and resident macrophages in the sciatic nerve during Wallerian degeneration and the following regeneration using immunohistochemistry. Sciatic nerves in Sprague-Dawley (SD) rats were examined after nerve crush. The rats were anesthetized with 100 mg of ketamine and 20 mg of xylazine in a dose of 1 ml/kg by intraperitoneal injection. Anti-ED-1 antibody was used to detect phagocytic macrophage and anti-OX-6 antibody was used to detect MHC class II cells. Few ED-1-immunopositive cells were seen within the normal sciatic nerve. After crush injury the number and the size of ED-1-immunopositive cells started to increase in all the segments distal to the crush site 3 days after injury and the number and size reached its peak on day 14 when the population of macrophage was 150 times higher in all the segments compared to controls. However, the number of ED-1-immunopositive cells and the size of the cells remains significantly high even after day 56 when functional recovery and axonal regeneration were complete. OX-6-immunopositive cells were observed within the control sciatic nerves. The number decreases significantly 3 days after injury in all the segments distal to the crush site but showed no significant difference thereafter. There were also no significant differences in the cell areas. ED-1-immunopositive phagocytic macrophages show significant differences temporally in both the cell number and the size even after axonal regeneration.

Animals↗
PubMed1980

Impaired retrograde axonal transport from a nerve crush in streptozotocin diabetic rats.

The axonal transport of proteins in crushed nerves of streptozotocin (40 mg/kg) diabetic rats was investigated 4 weeks after induction of diabetes. 35S-methionine was used as a marker for protein and 3H-fucose as a marker for glycoprotein. The precursors were injected into the fifth lumbar spinal ganglion and the accumulation of TCA-insoluble activity proximal and distal to a sciatic nerve ligature was measured at different time intervals after application of a crush. The start of accumulation distal to the ligature was delayed by 1 hour for proteins as well as for glycoproteins. Furthermore, the total amount of accumulated protein after 19 h was decreased by 18% while the decrease was 21% for glycoprotein. By insulin treatment the differences could both be prevented and reversed after 3 days of normoglycaemia. These findings demonstrate an impaired response to a nerve crush and might be the explanation for the regenerative abnormalities of peripheral nerves in diabetes.

Animals↗
PubMed2001

Mice lacking tPA, uPA, or plasminogen genes showed delayed functional recovery after sciatic nerve crush.

Axonal outgrowth during peripheral nerve regeneration relies on the ability of growth cones to traverse through an environment that has been altered structurally and along a basal lamina sheath to reinnervate synaptic targets. To promote migration, growth cones secrete proteases that are thought to dissolve cell-cell and cell-matrix adhesions. These proteases include the plasminogen activators (PAs), tissue PA (tPA) and urokinase PA (uPA), and their substrate, plasminogen. PA expression and secretion are upregulated in regenerating mammalian sensory neurons in culture. After sciatic nerve crush in mice, there was an induction of PA mRNAs in the sensory neurons contributing to the crushed nerve and an upregulation of PA-dependent activity in crushed nerve compared with sham counterparts during nerve regeneration. To further assess the role of the PA system during peripheral nerve regeneration, PA-dependent activity as well as recovery of sensory and motor function in the injured hindlimb were assessed in wild-type, tPA, uPA, and plasminogen knock-out mice. Protease activity visualized by gel zymography showed that after nerve crush, the upregulation of PA activity in the tPA and uPA knock-out mice was delayed compared with wild-type mice. Recovery of sensory function was assessed by toe pinch, footpad prick, and the toe-spreading reflex. All knock-out mice demonstrated a significant delay in hindlimb response to these sensory stimuli compared with wild-type mice. For each modality tested, the uPA knock-out mice were the most dramatically affected, showing the longest delay to initiate a response. These studies clearly showed that PAs were necessary for timely functional recovery by regenerating peripheral nerves.

Animals↗
PubMed2002

Screening for differentially expressed genes in the rat inner retina and optic nerve after optic nerve crush.

Limited optic nerve crush is a model of diffuse mechanical axon injury, the most prevalent cause of secondary neurodegeneration after closed head neurotrauma. In this report, a protocol is presented which allows for the rapid screening of differential gene expression in the inner retina, as well as the optic nerve, in response to partial nerve crush. To prove the reliability of the method, prototypically, the differential expression profiles of three candidate genes (kinesin light chain, ferritin, RYB-A) were verified. The method seems to be suitable to address the question of how differential gene expression contributes to degeneration, survival and axonal repair after partial nerve crush.

Animals↗
PubMed1993

The neurotrophic analogue of ACTH(4-9) reduces the perineuronal microglial reaction after rat facial nerve crush.

Following peripheral nerve crush, microglial cells proliferate and migrate to motoneuron cell bodies of the injured nerves. Newly formed glial processes displace nerve terminals from the cell bodies. This process is known as synaptic stripping. In animal models of peripheral nerve diseases, the ACTH(4-9) analogue, ORG2766, was shown to facilitate axonal regeneration and to protect against experimental neuropathy. In the present study we examined the effect of ORG2766 on the microglial reaction. After facial nerve crush, rats were treated with either ORG2766 (75 micrograms/kg/48 h) or saline and were killed on day 2-6 after operation. Blind counting of the number of perineuronal glial cells in the facial nucleus was used to assess the effect of ORG2766 treatment on the microglial reaction. In the saline-treated animals the number of perineuronal glial cells per motoneuron cell body on the crushed side increased significantly. This number increased up to day 5 after operation and decreased significantly from day 5 to 6. After an initial increase in the peptide-treated animals, however, the number of perineuronal glial cells remained constant from day 3 onwards. Hence, on post-operation days 4 and 5, this number was significantly less than that seen in saline-treated animals. Microglial cells proliferate, presumably through signalling by injured motoneurons. It is suggested that the decrease in the number of perineuronal glial cells in the ORG2766-treated animals is the result of a peptide-induced reduction in the release of mediating signals/cytokines or, alternatively, increased protection of motoneurons by stress proteins. Further research should address the mechanism of action of ORG2766 in animal models of motoneuron disease.

Adrenocorticotropic Hormone↗
PubMed1990

Endoneurial microenvironment and acute nerve crush injury in the rat sciatic nerve.

In severe peripheral nerve ischemia in the rat, serial nerve blood flow (NBF) measurements have identified evidence of 'no reflow', a mechanism of continued fiber damage during reperfusion. It has been postulated that 'no reflow' also occurs in nerve compression due to direct mechanical or ischemic (if compression is prolonged) injury of microvessels, resulting in continuing nerve fiber damage. To address this question, we measured endoneurial blood flow (NBF), oxygen tension and pH at the site of an acute nerve crush injury. In further sets of experiments, NBF and endoneurial oxygen tension were examined before and after prolonged epochs of crush. NBF and MR (microvascular resistance) were not appreciably different than values obtained in control animals without intervening brief nerve crush. NBF was slightly higher and MR slightly lower 2 h after injury, but the difference was not statistically significant. No evidence of significant endoneurial hypoxia or acidosis was observed. Similarly, after more prolonged crush there was no significant oligemia or hypoxia. The studies provide no evidence that 'no reflow' occurs in crush injury even if the injury is maintained for a period of time known to induce 'no reflow' with severe ischemia. We suggest that nerve damage in crush, and possibly compression, more likely arises from direct mechanical injury of fibers.

Animals↗
PubMed1991

Effects of nerve crush and transection on mRNA levels for nerve growth factor receptor in the rat facial motoneurons.

We found that the level of nerve growth factor receptor (NGF-R) mRNA in facial motoneurons was increased after both facial nerve crushing and transection by means of in situ hybridization histochemistry. The increased level of NGF-R mRNA was maintained for at least 8 weeks after facial nerve transection, while facial nerve crushing caused only a transient increase. Thus, expression of NGF-R mRNA paralleled the axonal regeneration process. In addition, the increase of NGF-R mRNA with crushing was more pronounced than with transection from the 3rd to the 14th day after the insult.

Animals↗
PubMed1995

Peroneal motor nerve crush injury and hyperbaric oxygen effect.

The potential therapeutic effect of hyperbaric oxygen (HBO) after rat peroneal nerve crush was evaluated. Animals were given 100% oxygen at 2.5 atmosphere absolute for 90 minutes twice daily for 1 week and then once daily for 1 week. Edema increased in crushed nerves compared with control nerves, but no effect was associated with the administration of HBO. Gait analysis demonstrated injury at 1, 7, and 14 days after nerve crush, but no difference was found at 22 and 28 days after injury (analysis of variance: P < .001, 10 animals per group). Eight weeks after injury, nerve stimulation and muscle force measurements were 114 g for the injured group and 146 g for the control group (P < .001). There were no HBO-associated changes in gait parameter or nerve/muscle force measurements. This study demonstrated that rat peroneal nerve crush injury causes acute intraneural edema and temporary decrement of gait parameters. Elicited nerve stimulation demonstrated persistent loss of force 4 weeks after normalization of gait, but no HBO effect.

Acute Disease↗
PubMed1993

Early ultrastructural studies on local acid phosphatase activity in rat sciatic nerve after nerve crush.

Rat sciatic nerve was crushed at mid thigh level. 30 minutes up to 24 hours after the lesion, the nerve was excised, fixed, stained for acid phosphatase activity, and embedded in araldite. The nerve was cut lengthwise over a distance of 6 mm proximally and distally to the lesion and examined by electron microscopy. Not more than 30 minutes after damage fundamental changes were found to take place, with little difference between the proximal and the distal "stump". Changes affect the axon itself, the axolemma and the Schwann cell. In the axoplasm, structures not existent in normal axons became visible during the first hour. Acid phosphatase activity appeared in the endoplasmatic reticulum, vesicles and cisterns, along the axolemma, and in the Schwann cell. Enzyme filled vesicles were released from the Schwann cell into the axoplasm. Mitochondria were found in increasing numbers in the axoplasm next to the lesion, being mainly small and round in shape and prominent where various organelles and enzymes had accumulated. It is concluded that the axon itself is capable of enzyme activation and organelle production, and that there is a complex interaction between the Schwann cell and the axoplasm after nerve crush.

Acid Phosphatase↗
PubMed1989

Optic nerve crush modulates proliferation of rod precursor cells in the goldfish retina.

Tritiated thymidine ([3H]TdR) autoradiography revealed a correlation between the rate of cell proliferation of rod precursor cells in the outer nuclear layer (ONL) of the goldfish retina and the postoperative interval after crush of the optic nerve (ONC). Ten days after unilateral ONC there were more labeled nuclei in the ONL of the nerve-crushed retina than in the intact, contralateral retina of the same fish one day after single bilateral intraocular injections of [3H]TdR. From 15 to 25 days after ONC, however, fewer labeled nuclei were found in the ONL of nerve-crushed retinae than in controls, illustrating a decrease in the number of cells entering the S-phase of the cell cycle; by 35 days the differences had disappeared, demonstrating that cell birth recovered to normal. When examined one month after [3H]TdR injection, fewer labeled cells were present in the nerve-crushed retina at all postoperative intervals. Examination of the numbers of labeled cells at various postoperative periods following bilateral ONC, when one retina was examined one day and the other retina was examined one month after [3H]TdR administration revealed that the ratios of labeled cells between the two retinae varied as a function of time after ONC. Therefore, optic nerve crush appears to enhance the proportion of initially labeled cells in the ONL that are either fated to undergo further cell generation cycles or to die.

Animals↗
PubMed1994

Nerve crush injuries--a model for axonotmesis.

Nerve crush is a commonly used experimental model in the rat; however, a standard method of inducing this injury has not been defined. This study examined six crush techniques that are frequently used and characterized the subsequent nerve injury. Five types of nerve crush using a No. 5 jeweler's forceps and a sixth using a 30-s single crush with a serrated hemostat were studied in the posterior tibial nerve of the Lewis rat. Regeneration was evaluated using serial walking track assessments at 1, 2, 4, 6, and 8 weeks postoperatively. Nerve conduction studies and histological examination were performed at 2 days, 2 weeks, and 8 weeks. Blood-nerve barrier breakdown was observed at 2 days and recovered by 2 weeks. By 4 weeks normal walking track patterns were obtained in all groups. A pattern of Wallerian degeneration and axonal regeneration was noted at 2 weeks, with histological recovery in all groups by 8 weeks. Nerve crush, induced by any of the six methods tested, was similar and provides a reliable model of axonotmesis.

Animals↗
PubMed2005

Assessment of motoneuron death during development following neonatal nerve crush and Mg2+ treatment.

BACKGROUND: Sciatic nerve injury in neonatal rats impairs muscle recovery and significantly reduces the number of surviving motoneurons. We examined the rate of motoneuron death after sciatic nerve crush in neonatal rats, as well as the neuroprotective effect of systemic MgSO4 administration, by assessing the number of horseradish peroxidase -labelled motoneurons in the spinal cord ventral horn, after injecting EDL and TA muscles. MATERIAL/METHODS: Left sciatic nerve crush was performed on the 2nd postnatal day. MgSO4 (0.05 ml of 1 M solution/10 g body weight) was administered subcutaneously, daily for twelve days. Animals were examined for the number of motoneurons of EDL and TA muscles, in the spinal cord ventral horns at 14, 21, and 28 days postnatally (P) and adulthood. 24 h to 48 h after intramuscular HRP injection, the animals were perfused transcardially with a fixative containing glutaraldehyde. Serial sections of the spinal cords were cut and processed for Hanker-Yates staining, and the number of labeled motoneurons was measured under a camera lucida. RESULTS: Nerve crush resulted in 37% motoneuron survival at P14, 33% at P21, 28% at P28 and 21% in adult rats. Following MgSO4 administration motoneuron survival rates of 51%, 47%, 44% and 39% were observed respectively, for the different age groups. The values obtained in magnesium-treated rats proved to be significantly different (p<0.05), compared to non-treated rats of the same age group. CONCLUSIONS: Nerve crush after birth resulted in significant motoneuron death, established already at P14. MgSO4 administration induced significant motoneuron survival.

Animals↗