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Nerve Section (nerve + section)
Selected AbstractsEph/ephrin expression in the adult rat visual system following localized retinal lesions: localized and transneuronal up-regulation in the retina and superior colliculusEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2005J. Rodger Abstract Following unilateral optic nerve section in adult PVG hooded rat, the axon guidance cue ephrin-A2 is up-regulated in caudal but not rostral superior colliculus (SC) and the EphA5 receptor is down-regulated in axotomised retinal ganglion cells (RGCs). Changes occur bilaterally despite the retino-collicular projection being mostly crossed. Here we investigate the dynamics of Eph/ephrin expression using in situ hybridization and semi-quantitative immunohistochemistry after localized retinal lesions. Unilateral krypton laser lesions to dorso-nasal retina ablated contralaterally projecting RGCs (DN group); ventro-temporal lesions ablated contralaterally and ipsilaterally projecting RGCs (VT group). Lesions of the entire retina served as controls (Total group). Results are compared to normal animals in which tectal ephrin-A2 and retinal EphA5 are expressed, respectively, as shallow ascending rostro-caudal and naso-temporal gradients. In both SCs of DN and Total groups, tectal ephrin-A2 was up-regulated caudally; in the VT group, expression remained normal bilaterally. Unilateral collicular ablation indicated that bilateral changes in ephrin-A2 expression are mediated via intercollicular pathways. EphA5 expression in the VT group was elevated in the intact nasal region of experimental retinae. For each experimental group, EphA5 expression was also elevated in nasal retina of the opposite eye, resulting in uniform expression across the naso-temporal axis. Up-regulation of ephrin-A2 in caudal, but not rostral, SC suggests the enhancement of developmental positional information as a result of injury. Bilateral increases in retinal EphA5 expression demonstrate that signals for up-regulation operate interocularly. The study demonstrates that signals regulating guidance cue expression are both localized and relayed transneuronally. [source] Expression of ephrin-A2 in the superior colliculus and EphA5 in the retina following optic nerve section in adult ratEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2001J. Rodger Abstract The vertebrate retina projects topographically to visual brain centres. In the developing visual system, gradients of ephrins and Eph receptors play a role in defining topography. At maturity, ephrins but not Ephs are downregulated. Here we show that optic nerve section in adult rat differentially regulates the expression of ephrin-A2 in the superior colliculus (SC) and of EphA5 in the retina. Expression was quantified immunohistochemically; ephrin-A2 levels were also estimated by semiquantitative reverse transcriptase polymerase chain reaction. In the normal SC, ephrin-A2 was expressed at low levels. At 1 month, levels of protein and of mRNA were upregulated across the contralateral SC giving rise to an increasing rostro-caudal gradient. At 6 months, levels had fallen but a gradient remained. In the retina of normal animals, EphA5 was expressed as an increasing naso-temporal gradient. By 1 month, expression was decreased in far temporal retina, resulting in a uniform expression across the naso-temporal axis. We suggest that denervation-induced plastic changes within the SC modify expression of these molecules. [source] Deafferentation-induced apoptosis of neurons in thalamic somatosensory nuclei of the newborn rat: critical period and rescue from cell death by peripherally applied neurotrophinsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2000Alfonso Baldi Abstract This study shows that unilateral transection of the infraorbital nerve (ION) in newborn (P0) rats induces apoptosis in the contralateral ventrobasal thalamic (VB) complex, as evidenced by terminal transferase-mediated deoxyuridine triphosphate-biotin nick end labelling (TUNEL) and electron miscroscopy. Double-labelling experiments using retrograde transport of labelled microspheres injected into the barrel cortex, followed by TUNEL staining, show that TUNEL-positive cells are thalamocortical neurons. The number of TUNEL-positive cells had begun to increase by 24 h postlesion, increased further 48 h after nerve section, and decreased to control levels after 120 h. Lesion-induced apoptosis in the VB complex is less pronounced if ION section is performed at P4, and disappears if the lesion is performed at P7. This time course closely matches the critical period of lesion-induced plasticity in the barrel cortex. Nerve growth factor (NGF) or brain-derived neurotrophic factor (BDNF), applied on the ION stump alone or in combination, are able to partially rescue thalamic neurons from apoptosis. Total cell counts in the VB complex of P7 animals that underwent ION section at P0 confirm the rescuing effect of BDNF and NGF. Blockade of axonal transport in the ION mimics the effect of ION section. These data suggest that survival-promoting signals from the periphery, maybe neurotrophins, are required for the survival of higher-order neurons in the somatosensory system during the period of fine-tuning of neuronal connections. We also propose that anterograde transneuronal degeneration in the neonatal rat trigeminal system may represent a new animal model for studying the pathways of programmed cell death in vivo. [source] Electrophysiological studies in a mouse model of Schwartz,Jampel syndrome demonstrate muscle fiber hyperactivity of peripheral nerve originMUSCLE AND NERVE, Issue 1 2009Andoni Echaniz-Laguna MD Abstract Schwartz,Jampel syndrome (SJS) is an autosomal-recessive condition characterized by muscle stiffness and chondrodysplasia. It is due to loss-of-function hypomorphic mutations in the HSPG2 gene that encodes for perlecan, a proteoglycan secreted into the basement membrane. The origin of muscle stiffness in SJS is debated. To resolve this issue, we performed an electrophysiological investigation of an SJS mouse model with a missense mutation in the HSPG2 gene. Compound muscle action potential amplitudes, distal motor latencies, repetitive nerve stimulation tests, and sensory nerve conduction velocities of SJS mice were normal. On electromyography (EMG), neuromyotonic discharges, that is, bursts of motor unit action potentials firing at high rates (120,300 HZ), were constantly observed in SJS mice in all muscles, except in the diaphragm. Neuromyotonic discharges were not influenced by general anesthesia and disappeared with curare administration. They persisted after complete motor nerve section, terminating only with Wallerian degeneration. These results demonstrate that perlecan deficiency in SJS provokes a neuromyotonic syndrome. The findings further suggest a distal axonal localization of the generator of neuromyotonic discharges. SJS should now be considered as an inherited disorder with peripheral nerve hyperexcitability. Muscle Nerve, 2009 [source] The effect of vestibular nerve section upon tinnitusCLINICAL OTOLARYNGOLOGY, Issue 4 2002D.M. Baguley This paper reviews the published evidence regarding the effect of vestibular nerve section upon tinnitus. This is of relevance not only for those performing and undergoing this procedure, but also for those considering the hypothesis that auditory efferent system dysfunction may be influential in tinnitus perception. The auditory medial efferent fibres within the internal auditory canal run within the inferior vestibular nerve, only joining the cochlear nerve at the anastomosis of Oort, a bundle of 1300 fibres running from the saccular branch of the inferior vestibular nerve to the cochlear nerve. Vestibular nerve section procedures therefore section this efferent olivocochlear pathway, and ablate efferent influence upon that cochlear. If auditory efferent dysfunction is involved in tinnitus perception, this ablation might influence the tinnitus status of that patient. A literature search identified 18 papers mentioning tinnitus status after vestibular nerve section, describing the experiences of a total of 1318 patients. The proportion of patients in whom tinnitus was said to be exacerbated postoperatively ranged from 0% to 60%, with a mean of 16.4% (standard deviation 14.0). The proportion of patients in whom tinnitus was unchanged was 17% to 72% (mean 38.5%, standard deviation 15.6), and in whom tinnitus was said to be improved was 6% to 61% (mean 37.2%, standard deviation 15.2). In the majority of patients undergoing this procedure, ablation of auditory efferent input (and thus total efferent dysfunction) to the cochlea was not associated with an exacerbation of tinnitus. The finding of this review is that efferent dysfunction after vestibular nerve section does not consistently worsen tinnitus. [source] Neural cell adhesion molecule expression: No correlation with perineural invasion in cutaneous squamous cell carcinoma of the head and neckHEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 6 2009C. Arturo Solares MD Abstract Background. Perineural invasion (PNI) in cutaneous squamous cell carcinoma of the head and neck (CSCCHN) is associated with decreased survival, particularly in patients with clinical signs of cranial nerve involvement. There is evidence to indicate that neural cell adhesion molecule (N-CAM) confers capability of PNI. We analyzed our own patient population to determine if N-CAM predicted clinical PNI in CSCCHN. Methods. Tissue from patients with CSCCHN and clinical PNI, who underwent surgery between 1998 and 2005, was immunostained for N-CAM. In addition, non-PNI CSCCHN and normal nerve sections were also stained. A section of neuroendocrine tumor was included in each slide as a positive control. In addition, most of the sections also had an "inbuilt control" in the CD56 positive natural killer T cells that formed part of the inflammatory reaction to the tumors. Results. Tissue was available from 14 patients with CSCCHN and clinical PNI. The analysis was carried out in 14 patients without PNI and 4 normal nerves. N-CAM was not expressed in any of our PNI CSCCHN specimens or non-PNI controls. It was strongly expressed in the neuroendocrine tumors and positive in-built controls, as well as in normal nerve tissue. Conclusion. N-CAM expression did not predict neurotropism in our patient population. Additional studies are required to identify the cell surface markers expressed by CSCCHN which confer neurotropism capabilities. © 2009 Wiley Periodicals, Inc. Head Neck, 2009 [source] Development of the blood-nerve barrier in neonatal ratsMICROSURGERY, Issue 7 2001Christopher E. Smith M.D. The blood-nerve barrier (BNB) is constituted by the perineurium and the endothelium of endoneurial microvessels. We investigated the age at which the vascular component of BNB function is established in the rat and the ultrastructural modifications accompanying changes in permeability. BNB permeability was assessed with injections of Evans blue albumin (EBA) and horseradish peroxidase (HRP) in rats of different ages. Sciatic nerve sections were studied using fluorescence and electron microscopy. Nerves from animals injected with EBA indicated that the BNB is not functional before 13 days of life but that its function is established by 16 days. These results were confirmed by electron microscope examination of nerve sections from animals injected with HRP, which showed clefts between the endothelial cells of endoneurial vessels in young rats. In rats over 18 days, these clefts were occluded by tight junctions, which prevented HRP from leaving the vessel lumen and conferred BNB function. Systematic morphometric analysis of nerves from different age groups allowed the establishment of baseline normal histologic neural development with age. © 2001 Wiley-Liss, Inc. MICROSURGERY 21:290,297 2001 [source] Supraspinal control of external anal sphincter motility: effects of vesical distension in humans and catsNEUROGASTROENTEROLOGY & MOTILITY, Issue 11 2006V. Vitton Abstract, A pontine centre located near the micturition centre controlling external anal sphincter (EAS) motility via noradrenergic neurones has been described in cats. The aim of this study was to determine (i) whether a similar centre controls EAS motility in humans and (ii) whether this centre is involved in vesico-sphincteric reflexes in cats and humans. The effects of an alpha-1-adrenoceptor antagonist (nicergoline) and those of vesical distension on the electrical activity of the EAS were studied in paraplegic and non-paraplegic volunteers. The effects of vesical distension by injecting saline at physiological levels on the responses of the EAS to pudendal nerve stimulation were investigated in intact cats and cats with nerve sections. In non-paraplegic subjects, nicergoline and vesical distension abolished the activity of the EAS. These effects were no longer observed in paraplegic patients. In cats, vesical distension inhibited the reflex response of the EAS to pudendal nerve stimulation. This vesico-sphincteric reflex, which was no longer observed in spinal animals, persisted after nicergoline injection. These findings indicate that in humans, there exists a supra-spinal centre facilitating the tonic activity of the EAS via noradrenergic neurones not involved in the inhibitory vesico-sphincteric reflex. [source] The Critical Role of IL-12p40 in Initiating, Enhancing, and Perpetuating Pathogenic Events in Murine Experimental Autoimmune NeuritisBRAIN PATHOLOGY, Issue 4 2002Lei Bao Interleukin 12 (IL-12) is a proinflammatory cytokine with important immunoregulatory activities and is critical in determining the differentiation and generation of Th1 cells. For the present study, we investigated the role of endogenous IL-12 in the pathogenesis of experimental autoimmune neuritis (EAN), which is a CD4+ T-cell mediated autoimmune inflammatory disease of the peripheral nervous system. EAN is used as an animal model for Guillain-Barré syndrome of humans. Here, EAN was established in IL-12 p40 deficient mutant (IL-12 -/- ) C57BL/6 mice by immunization with P0 peptide 180,199, a purified component of peripheral nerve myelin, and Freund's complete adjuvant. In these IL-12 -/- mice the onset of clinical disease was delayed, and the incidence and severity of EAN were significantly reduced compared to that in wild-type mice. The former group's clinical manifestations were associated with less P0-peptide 180,199 induced secretion of interferon-, (IFN-,) by splenocytes in vitro and low production of anti-P0-peptide 180,199 IgG2b antibodies in serum. Fewer IFN-, and TNF-, producing cells, but more cells secreting IL-4, were found in sciatic nerve sections from IL-12 -/- mice, consistent with impaired Th1 functions and response. However, the IL-12 deficiency appeared not to affect P0 peptide 180,199-specific T-cell proliferation. These results indicate that IL-12 has a major role in the initiation, enhancement and perpetuation of pathogenic events in EAN by promoting a Th1 cell-mediated immune response and suppressing the Th2 response. This information augments consideration of IL-12 as a therapeutic target in Guillain-Barré syndrome and other T-cell-mediated autoimmune diseases. [source] | ||||||||||