Home About us Contact
|
Home About us Contact | ||
|
|
||
Myelinated Fibres (myelinated + fibre)
Selected AbstractsDiet-induced obesity in Sprague,Dawley rats causes microvascular and neural dysfunctionDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 4 2010Eric P. Davidson Abstract Background The objective of this study was to determine the effect of diet-induced obesity (DIO) on microvascular and neural function. Methods Rats were fed a standard or high fat diet for up to 32 weeks. The following measurements were carried out: vasodilation in epineurial arterioles using videomicroscopy, endoneurial blood flow using hydrogen clearance, nerve conduction velocity using electrical stimulation, size,frequency distribution of myelinated fibres of the sciatic nerve, intraepidermal nerve fibre density using confocal microscopy and thermal nociception using the Hargreaves method. Results Rats fed a high fat diet for 32 weeks developed sensory neuropathy, as indicated by slowing of sensory nerve conduction velocity and thermal hypoalgesia. Motor nerve conduction velocity and endoneurial blood flow were not impaired. Mean axonal diameter of myelinated fibres of the sciatic nerve was unchanged in high fat-fed rats compared with that in control. Intraepidermal nerve fibre density was significantly reduced in high fat-fed rats. Vascular relaxation to acetylcholine and calcitonin gene-related peptide was decreased and expression of neutral endopeptidase (NEP) increased in epineurial arterioles of rats fed a high fat diet. In contrast, insulin-mediated vascular relaxation was increased in epineurial arterioles. NEP activity was significantly increased in the skin of the hindpaw. Markers of oxidative stress were increased in the aorta and serum of high fat-fed rats but not in epineurial arterioles. Conclusion Chronic obesity causes microvascular and neural dysfunction. This is associated with increased expression of NEP but not oxidative stress in epineurial arterioles. NEP degrades vasoactive peptides, which may explain the decrease in microvascular function. Copyright © 2010 John Wiley & Sons, Ltd. [source] Endogenous BDNF is required for myelination and regeneration of injured sciatic nerve in rodentsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2000Jian-Yi Zhang Abstract Following a peripheral nerve injury, brain-derived neurotrophic factor (BDNF) and the p75 neurotrophin receptor are upregulated in Schwann cells of the Wallerian degenerating nerves. However, it is not known whether the endogenous BDNF is critical for the functions of Schwann cells and regeneration of injured nerve. Treatment with BDNF antibody was shown to retard the length of the regenerated nerve from injury site by 24%. Histological and ultrastructural examination showed that the number and density of myelinated axons in the distal side of the lesion in the antibody-treated mice was reduced by 83%. In the BDNF antibody-treated animals, there were only distorted and disorganized myelinated fibres in the injured nerve where abnormal Schwann cells and phagocytes were present. As a result of nerve degeneration in BDNF antibody-treated animals, subcellular organelles, such as mitochondria, disappeared or were disorganized and the laminal layers of the myelin sheath were loosened, separated or collapsed. Our in situ hybridization revealed that BDNF mRNA was expressed in Schwann cells in the distal segment of lesioned nerve and in the denervated muscle fibres. These results indicate that Schwann cells and muscle fibres may contribute to the sources of BDNF during regeneration and that the deprivation of endogenous BDNF results in an impairment in regeneration and myelination of regenerating axons. It is concluded that endogenous BDNF is required for peripheral nerve regeneration and remyelination after injury. [source] Abnormal substance P release from the spinal cord following injury to primary sensory neuronsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2000Marzia Malcangio Abstract The neuropeptide substance P (SP) modulates nociceptive transmission within the spinal cord. Normally, SP is uniquely contained in a subpopulation of small-calibre axons (A,- and C-fibres) within primary afferent nerve. However, it has been shown that after nerve transection, besides being downregulated in small axons, SP is expressed de novo in large myelinated A,-fibres. In this study we investigated whether, following peripheral nerve injury, SP was released de novo from the spinal cord after selective activation of A,-fibres. Spinal cords with dorsal roots attached were isolated in vitro from rats 2 weeks following distal sciatic axotomy or proximal spinal nerve lesion (SNL). The ipsilateral dorsal roots were electrically stimulated for two consecutive periods at low- or high-threshold fibre strength, spinal cord superfusates were collected and SP content was determined by radioimmunoassay. SNL, but not axotomized or control rat cords, released significant amounts of SP after selective activation of A,-fibres. Not only do these data support the idea that A, myelinated fibres contribute to neuropathic pain by releasing SP, they also illustrate the importance of the proximity of the lesion to the cell body. [source] Dejerine-Sottas Neuropathy with Multiple Nerve Roots Enlargement and Hypomyelination Associated with a Missense Mutation of the Transmembrane Domain of MPZ/P0JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2003A Simonati In a patient affected with a slowly progressive, severe form of Dejerine-Sottas syndrome, symmetric enlargement of cranial nerves and focal hypertrophy of cervical and caudal roots were detected following MRI. Neuropathological features of the sural nerve disclosed a dramatic loss of myelinated fibres, with skewed-to-the-left, unimodal distribution of the few residual fibres, consistent with the diagnosis of congenital hypomyelination neuropathy. Genetic analysis revealed this condition to be associated with a heterozygous G to A transition at codon 167 in the exon 4 of the MPZ/P0 gene causing a Gly138Arg substitution in the transmembrane domain of the mature MPZ/P0 protein. Focal enlargement of the nerve trunks in demyelinating, hereditary motor and sensory neuropathies (HMSN) was previously reported in both asymptomatic and symptomatic cases with root compression, but peculiar to this case is the diffuse involvement of both cranial and spinal nerves. We believe that the relevance of nerve trunk hypertrophy in HMSN is probably underevaluated: therefore MRI investigation of the head and spine should be included in the diagnostic study of selected HMSN patients. Molecular analysis of peripheral myelin genes will help to rule out misdiagnosed cases. [source] Involvement of the auditory brainstem system in spinocerebellar ataxia type 2 (SCA2), type 3 (SCA3) and type 7 (SCA7)NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 5 2008F. Hoche Aims: The spinocerebellar ataxia type 2 (SCA2), type 3 (SCA3) and type 7 (SCA7) are clinically characterized by progressive and severe ataxic symptoms, dysarthria, dysphagia, oculomotor impairments, pyramidal and extrapyramidal manifestations and sensory deficits. Although recent clinical studies reported additional disease signs suggesting involvement of the brainstem auditory system, this has never been studied in detail in SCA2, SCA3 or SCA7. Methods: We performed a detailed pathoanatomical investigation of unconventionally thick tissue sections through the auditory brainstem nuclei (that is, nucleus of the inferior colliculus, nuclei of the lateral lemniscus, superior olive, cochlear nuclei) and auditory brainstem fibre tracts (that is, lateral lemniscus, trapezoid body, dorsal acoustic stria, cochlear portion of the vestibulocochlear nerve) of clinically diagnosed and genetically confirmed SCA2, SCA3 and SCA7 patients. Results: Examination of unconventionally thick serial brainstem sections stained for lipofuscin pigment and Nissl material revealed a consistent and widespread involvement of the auditory brainstem nuclei in the SCA2, SCA3 and SCA7 patients studied. Serial brainstem tissue sections stained for myelin showed loss of myelinated fibres in two of the auditory brainstem fibre tracts (that is, lateral lemniscus, trapezoid body) in a subset of patients. Conclusions: The involvement of the auditory brainstem system offers plausible explanations for the auditory impairments detected in some of our and other SCA2, SCA3 and SCA7 patients upon bedside examination or neurophysiological investigation. However, further clinical studies are required to resolve the striking discrepancy between the consistent involvement of the brainstem auditory system observed in this study and the comparatively low frequency of reported auditory impairments in SCA2, SCA3 and SCA7 patients. [source] Farber's disease diagnosed by nerve biopsyNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 2 2002J. Jacobs Introduction:, Farber's disease (granulomatosis) is a rare inherited lipid storage disease caused by a deficiency of lysosomal acid-ceramidase. Clinical features include contractures of limbs with swelling of joints and multiple subcutaneous nodules. In a few cases there is prominent involvement of central and peripheral nervous systems. Ceramide accumulates in the nodules and in cells of many other tissues including brain. Electron microscopy of affected cells shows membrane-bound inclusions, some of which have a highly characteristic curved or ,banana' shape (Farber bodies). Nerve biopsy findings have been described in a few cases but our patient appears to be the first to have been diagnosed by nerve biopsy. Case report:, This male infant presented at 6 months with joint pain and swelling, fever weakness and nystagmus: EMNG demonstrated sensory-motor polyneuropathy with features of demyelination. Semi-thin resin sections show a moderately reduced density of myelinated fibres. The myelin sheaths of most fibres are inappropriately thin, which was confirmed morphometrically: some axons are demyelinated. Vacuolar inclusions are seen in some Schwann cells. Teased fibres show de- and remyelination. Electron microscopy shows oval, boomerang- or banana-shaped inclusions in Schwann cells associated with myelinated and unmyelinated axons, but not in other cell types. Conclusion:, Farber's disease is associated with a demyelinating neuropathy. [source] Structural and Ultrastructural Study of the Intracranial Portion of the Oculomotor, Trochlear and Abducent Nerves in DogANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 3 2006J. Vivo Summary The right intracranial portion of the oculomotor, trochlear and abducent nerves were removed from six adult German shepherd dogs and analysed by light and electron microscopy. In all cases the nerve sectional area was calculated. Unmyelinated and myelinated fibres were analysed and number, diameter and cross-sectional area were calculated. In myelinated fibres, also calculated were the corresponding axon area and diameter, and myelin sheath thickness. The mean number of myelinated fibres was 8543.50 ± 1231.85 being the unmyelinated 1402 ± 241.58 in the oculomotor nerve; 1509 ± 223.17 and 287.67 ± 72.28 in the trochlear nerve and 2473.00 ± 211.41 and 231.25 ± 92.67 respectively in the abducent. The mean diameter was 10.23 ± 0.68 ,m in myelinated and 0.43 ± 0.21 for unmyelinated in oculomotor nerve, 10.53 ± 0.55 ,m and 0.33 ± 0.04 for the trochlear, and 10.45 ± 1.27 ,m and 0.47 ± 0.09 in the abducent nerve respectively. This study reveals that oculomotor, trochlear and abducent nerves of the dog show structural and ultra-structural features similar to the same nerves in other species. [source] Pulmonary function tests and diaphragmatic compound muscle action potential in patients with sporadic amyotrophic lateral sclerosisACTA NEUROLOGICA SCANDINAVICA, Issue 6 2010T. N. Sathyaprabha Sathyaprabha TN, Pradhan C, Nalini A, Thennarasu K, Raju TR. Pulmonary function tests and diaphragmatic compound muscle action potential in patients with sporadic amyotrophic lateral sclerosis. Acta Neurol Scand: 2010: 121: 400,405. © 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Background,,, Respiratory failure is the primary cause of death in patients with amyotrophic lateral sclerosis (ALS). Diaphragmatic compound muscle action potentials (DCMAP) are valid parameters to assess the respiratory muscle innervation. Aim,,, In this study we propose to establish evidence of pulmonary dysfunction in patients with ALS and its relation to DCMAP parameters among patients with sporadic ALS. Materials and methods,,, Twenty nine patients (M-20, F-9) diagnosed to have sporadic ALS by El. Escorial criteria, without symptoms of pulmonary dysfunction, and able to perform the PFT satisfactorily, were studied. Thirty controls (M-20, F-10) were selected from patient's relatives. Forced vital capacity (FVC), forced expiratory volume in one second (FEV1), peak expiratory flow rate (PEFR) and maximum voluntary ventilation (MVV) were measured by spirometry. Maximum expiratory pressure (MEP) was measured by digital peak pressure monitor. Right phrenic nerve conductions (DCMAP) were performed and the latencies and amplitude of diaphragmatic com-pound action potential (DCMAP) was recorded in controls and ALS patients. Results,,, The mean age of patients was 51.41 ± 10.72 years (37,82) and control was 53.57 ± 8.85 years (30,68). None of the patients had symptoms or clinical evidence of respiratory dysfunction. The FVC, FEV1, PEFR, MVV, MIP and MEP were significantly (P < 0.001) reduced in ALS. The mean DCMAP amplitude was reduced among patients (610 ± 506.231 ,v) as compared to controls (1303.33 ± 584.56, P < 0.001) and mean latency was increased in patients (9.73 ± 2.57 ms) compared to controls (7.69 ± 0.87, P = 0.001). There was significant negative correlation between PFTs and latencies of DCMAP. Amplitude of DCMAP did not correlate with PFTs. Conclusion,,, There is significant negative correlation between DCMAP latencies and PFTs suggesting early loss of myelinated fibres and diaphragmatic dysfunction. DCMAP latencies may be a good indicator of early respiratory muscle involvement and also of disease progression in ALS. [source] | |||||||||||||