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Unmyelinated Fibers (unmyelinated + fiber)
Selected AbstractsTransthyretin enhances nerve regenerationJOURNAL OF NEUROCHEMISTRY, Issue 2 2007Carolina E. Fleming Abstract Mutations in transthyretin (TTR) are associated with familial amyloid polyneuropathy, a neurodegenerative disorder characterized by TTR deposition in the PNS. The aim of this study was to unravel whether TTR has a role in nerve physiology that could account for its preferential accumulation in the PNS, when mutated. The sensorimotor performance of wild-type and TTR knockout (KO) littermate mice was compared and showed impairment in mice lacking TTR. Given the possibility that, upon regeneration, the consequences arising from TTR absence might be exacerbated, nerve crush was performed in both strains. TTR KO mice presented delayed functional recovery resulting from decreased number of myelinated and unmyelinated fibers. Moreover, in transgenic mice in a TTR KO background, expressing human TTR in neurons, this phenotype was rescued, reinforcing that TTR enhances nerve regeneration. In vitro assays showed that neurite outgrowth and extension were decreased in the absence of TTR, probably underlying the decreased number of regenerating axons in TTR KO mice. Our findings demonstrate that TTR participates in nerve physiology and that it enhances nerve regeneration. Moreover, the assignment of a TTR function in nerve biology and repair, may explain its preferential deposition, when mutated, in the PNS of familial amyloid polyneuropathy patients. [source] Immunohistochemical and electron microscopic study of invasion and differentiation in spinal cord lesion of neural stem cells grafted through cerebrospinal fluid in ratJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2002Sufan Wu Abstract Neurospheres were obtained by culturing hippocampal cells from transgenic rat fetuses (E16) expressing green fluorescent protein (GFP). The neurosphere cells were injected into the cerebrospinal fluid (CSF) through the 4th ventricle of young rats (4 weeks old) that had been given a contusion injury at T8,9 of the spinal cord. The injected neural stem cells were transported through the CSF to the spinal cord, attached to the pial surface at the lesion, and invaded extensively into the spinal cord tissue as well as into the nerve roots. The grafted stem cells survived well in the host spinal cord for as long as 8 months after transplantation. Immunohistochemical study showed that many grafted stem cells had differentiated into astrocytes at 1,4 months, and some into oligodendrocytes at 8 months postoperatively. Immunoelectron microscopy showed that the grafted stem cells were well integrated into the host tissue, extending their processes around nerve fibers in the same manner as astrocytes. In addition, grafted stem cells within nerve roots closely surrounded myelinated fibers or were integrated into unmyelinated fiber bundles; those associated with myelinated fibers formed basal laminae on their free surface, whereas those associated with unmyelinated fibers were directly attached to axons and Schwann cells, indicating that grafted stem cells behaved like Schwann cells in the nerve roots. © 2002 Wiley-Liss, Inc. [source] Phrenic nerve diabetic neuropathy in rats: unmyelinated fibers morphometryJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2009Valéria Paula S. Fazan Abstract We have demonstrated that phrenic nerves' large myelinated fibers in streptozotocin (STZ)-induced diabetic rats show axonal atrophy, which is reversed by insulin treatment. However, studies on structural abnormalities of the small myelinated and the unmyelinated fibers in the STZ-model of neuropathy are limited. Also, structural changes in the endoneural vasculature are not clearly described in this model and require detailed study. We have undertaken morphometric studies of the phrenic nerve in insulin-treated and untreated STZ-diabetic rats and non-diabetic control animals over a 12-week period. The presence of neuropathy was assessed by means of transmission electron microscopy, and morphometry of the unmyelinated fibers was performed. The most striking finding was the morphological evidence of small myelinated fiber neuropathy due to the STZ injection, which was not protected or reversed by conventional insulin treatment. This neuropathy was clearly associated with severe damage of the endoneural vessels present on both STZ groups, besides the insulin treatment. The STZ-diabetes model is widely used to investigate experimental diabetic neuropathies, but few studies have performed a detailed assessment of either unmyelinated fibers or capillary morphology in this animal model. The present study adds useful information for further investigations on the ultrastructural basis of nerve function in diabetes. [source] Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 21JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003R Bianchi Erythropoietin (EPO) has neurotrophic and neuroprotective effects and its efficacy and safety has been demonstrated in patients with ischemic stroke. We investigated its efficacy in preventing and reversing established nerve disorders in streptozotocin (STZ) diabetes. After STZ injection (60 mg/kg/ip), EPO (5000 units/kg b.w. i.p. three times a week) was started in a group of rats and continued for five weeks (prevention schedule). In another group of diabetic rats, EPO was started six weeks after STZ, continued for five weeks (therapeutic schedule). Groups of non-diabetic control rats were similarly treated. Antidromic nerve conduction velocity (NCV) in the tail was assessed at five weeks for all groups and at 11 weeks for the therapeutic schedule. Compared to non-diabetic rats, NCV was 21% lower (P < 0.001) at five weeks in the STZ group, EPO partially prevented this decrease (14% lower than with non-diabetic controls), with a significant difference from the untreated-diabetic group (P < 0.01). After six weeks of uncontrolled diabetes, at the beginning of therapeutic EPO, NCV was reduced by 23% and after 11 weeks by 40%, EPO efficacy was confirmed. Thermal (hot plate method) and mechanical (Randall-Selitto method) nociceptive thresholds were monitored weekly throughout the study. In addition, in all groups, the density of intra-epidermal nerve fibers, which reflects possible degeneration of somatic unmyelinated fibers, was assessed in the hindpaw using protein-gene-product 9.5 immunostaining. Rats developed mechanical hyperalgesia within two weeks after STZ injection. Both the prevention and therapeutic schedules of EPO reduced diabetic hyperalgesia after two weeks of treatment, reaching statistical significance at fur, and five weeks of treatment, with no such effect in non-diabetic controls. Hindpaw thermal response latencies were significantly (P < 0.001) increased in untreated diabetic rats compared with untreated controls. EPO had no effect on these latencies in control rats but partially prevented the increase in diabetic rats, so the values were still different from controls, but significantly different from untreated diabetics at four and five weeks in both the prevention and therapeutic studies (P < 0.05). These observations extend the therapeutic utility of EPO and highlight its potential for treating established diabetic neuropathies. [source] Peripheral neuropathy associated with mitochondrial disorders: 8 cases and review of the literatureJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 4 2002S. Bouillot Abstract Forty-three cases of peripheral neuropathy (PN) have been reported in the literature with a proven mitochondria (mt) DNA mutation, and 21 had a peripheral nerve biopsy (PNB). We studied 8 patients, 1 of whom had severe sensory PN, 3 mild PN, and 4 subclinical PN. Nerve biopsy was performed in every case; all patients showed axonal degeneration and 4 showed features of primary myelin damage. In addition, there were 2 crystalline-like inclusions in the Schwann cell cytoplasm of a patient with MERRF, and 1 in a patient with multiple deletions on the mtDNA. There are 11 cases of PNB in the literature with axonal lesions, 5 with demyelination, and 4 with mixed lesions. One PNB was not modified. A few crystalline-like inclusions were seen in 1 case of MERRF. Such inclusions were first reported in the Schwann cell cytoplasm of unmyelinated fibers in a patient with Refsum disease and were considered to be modified mitochondria. However, their mitochondrial origin remains debatable. [source] A FAMILY WITH AUTOSOMAL DOMINANT MUTILATING NEUROPATHY NOT LINKED TO EITHER 3q13-q22 OR 9q22 LOCIJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2000E. Bellone The clinical separation of CMT2 from HSAN I may be difficult in some kindreds in which the sensory and motor symptoms and deficits are approximately alike. The genetic studies of CMT2 families are also controversial: one form of CMT2 was shown to map on chromosome 3q13-q22 and named CMT2B; the HSAN I locus was mapped to 9q22.1. We describe a family with an autosomal dominant inheritance in which at least three members, belonging to three generations, developed a progressive neuropathy that combined limb weakness, wasting, and severe distal sensory loss leading to prominent mutilating changes. The onset was in late childhood, with progressive weakness in the lower limbs and later in the hands, resulting in a severe paralysis in the feet in one patient. Sensory disturbances were pronounced in 2 patients, and led to poorly healing ulcerations with osteomyelitis and amputations in one foot and mutilating lesions of both hands. Electrophysiological investigation revealed an axonopaty with consistent motor damage. Sural nerve biopsy showed a reduction in the density of both myelinated and unmyelinated fibers, with regenerating clusters. Linkage analysis using 5 microsatellite markers within to the critical 9q22 region was performed. Lod scores of this family calculated by LINKAGE package excluded association to this locus. We also performed linkage studies with chr. 3q13-q22 markers associated to the CMT2b locus. Lod scores excluded this locus as well as responsiblity of the familial phenotype. The severity of motor involvement would suggest classifying the disorder of this family as a form of HSMN II rather than HSAN, indicating that a new locus is involved in the pathogenesis of this disorder. [source] Demyelination Induces the Decline of the Myelinated Fiber Length in Aged Rat White MatterTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 4 2009Chen Li Abstract To determine the exact reason for the age-related decline of the myelinated fiber length in white matter, we performed this study. In middle-aged rats, there was age-related loss of the unmyelinated fibers with large diameters. The demyelination of the myelinated fibers with small diameters in middle-aged rat white matter might make the age-related decrease of the unmyelinated fibers with small diameters in the white matter unnoticeable. However, in old-aged female rats, the unmyelinated fibers with large and small diameters significantly degenerated together and that the unmyelinated fibers formed from the demyelination of the myelinated fibers could not replenish the age-related loss of the unmyelinated fibers in the white matter. In conclusion, this study suggested that demyelination of myelinated fibers with small diameters in aged white matter might be the key mechanism of the significant decline of the myelinated fiber length in aged white matter. Anat Rec, 292:528,535, 2009. © 2009 Wiley-Liss, Inc. [source] | ||||||||||