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Rat Optic Nerve (rat + optic_nerve)
Selected AbstractsConduction block and glial injury induced in developing central white matter by glycine, GABA, noradrenalin, or nicotine, studied in isolated neonatal rat optic nerveGLIA, Issue 11 2009Stavros Constantinou Abstract The damaging effects of excessive glutamate receptor activation have been highlighted recently during injury in developing central white matter. We have examined the effects of acute exposure to four other neurotransmitters that have known actions on white matter. Eighty minutes of Glycine or GABA-A receptor activation produced a significant fall in the compound action potential recorded from isolated post-natal day 10 rat optic nerve. This effect was largely reversed upon washout. Nicotinic acetylcholine receptor (nAChR) or adrenoreceptor activation with noradrenalin resulted in an ,35% block of the action potential that did not reverse during a 30-min washout period. While the effect of nAChR activation was blocked by a nAChR antagonist, the effect of noradrenalin was not ablated by ,- or ,-adrenoreceptor blockers applied alone or in combination. In the absence of noradrenalin, co-perfusion with ,- and ,-adrenoreceptor blockers resulted in nonreversible nerve failure indicating that tonic adrenoreceptor activation is required for nerve viability, while overactivation of these receptors is also damaging. Nerves exposed to nAChR + adrenoreceptor activation showed no axon pathology but had extensive glial injury revealed by ultrastructural analysis. Oligodendroglia exhibited regions of membrane vacuolization while profound changes were evident in astrocytes and included the presence of swollen and expanded mitochondria, vacuolization, cell processes disintegration, and membrane breakdown. Blinded assessment revealed higher levels of astrocyte injury than oligodendroglial injury. The findings show that overactivation of neurotransmitter receptors other than those for glutamate can produce extensive injury to developing white matter, a phenomenon that may be clinically significant. © 2009 Wiley-Liss, Inc. [source] Thrombin attenuation is neuroprotective in the injured rat optic nerveJOURNAL OF NEUROCHEMISTRY, Issue 3 2001Igor Friedmann The functional loss that often follows injury of the mammalian CNS has been attributed not only to the immediate neural loss, but also to secondary neuronal degeneration caused by toxic biochemical mediators in the environment of the injured nerve. We report here that a high thrombin content, produced as a result of injury-induced activation of prothrombin, appears to be an important mediator of secondary damage. Measurement of post-traumatic neuronal survival in vivo revealed that post-traumatic local application of the thrombin inhibitor N -,-(2-naphthylsulphonylglycyl)-4-(d,l)-amidinophenylalanine piperidide acetate in the rat optic nerve subjected to mild partial crush injury left twice as many retinal ganglion cells with functioning axons as in controls. Thus, by readjusting thrombin activity, thereby possibly obtaining a moderate post-traumatic increase and thus gaining the benefit of thrombin without its toxic effects, it may be possible to create an environment that is more favourable towards post-traumatic survival. [source] Methylprednisolone exacerbates axonal loss following optic nerve trauma in ratsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2002KD Steinsapir PURPOSE: This study investigates the clinical dogma that very high doses of methylprednisolone helpful in spinal cord injury are also helpful in optic nerve trauma. Methods: The right optic nerve of 29 male rats received a 5 second traumatic crush followed 30 minutes later by one of five intravenous treatments (methylprednisolone 30 mg/kg, 60 mg/kg, 90 mg/kg, 120 mg/kg, or saline). Treatment was continued for three additional administrations at 6 hour intervals. Untreated sham controls (n = 7) were also prepared. Six weeks after injury, animals were sacrificed, perfused and optic nerves systematically counted. RESULTS: Axon counts (means +/, s.e.m.) were as follows: Saline = 16,670 +/, 8,900 (n = 5); Methylprednisolone: 30 mg/kg = 8,098 +/, 4,741 (n = 5); 60 mg/kg = 6,925 +/, 6,517 (n = 4); 90 mg/kg = 2,663 +/, 2,653 (n = 4); 120 mg/kg = 6,149 +/, 3,487 (n = 6). Consequently, the data revealed that saline treated animals retained more axons than those that were administered methylprednisolone (p < 0.02). CONCLUSIONS: We conclude that methylprednisolone exacerbates axonal loss following crush injury in the rat optic nerve. Based on the results of this study, clinical studies of traumatic optic neuropathy in the future should also examine the possibility that corticosteroid treatment may have an adverse effect on visual outcome following optic nerve trauma. [source] Glutamate receptor-mediated ischemic injury of premyelinated central axons,ANNALS OF NEUROLOGY, Issue 5 2009James J.P. Alix Objective Ischemic injury of axons is a feature of periventricular leukomalacia, a pathological correlate of cerebral palsy. Recent evidence suggests that axons are damaged before they receive the first layer of compact myelin. Here we examine the cellular mechanisms underlying ischemic-type injury of premyelinated central axons. Methods Two-thirds of axons in the postnatal day 10 (P10) rat optic nerve are small premyelinated axons (<0.4,m in diameter), and one-third have undergone radial expansion in preparation for glial contact and the onset of myelination. Compound action potential recording and quantitative electron microscopy were used to examine the effect of modeled ischemia (oxygen-glucose deprivation) upon these two axon populations. Glutamate receptor (GluR) expression was investigated using polymerase chain reaction (PCR) and immunostaining approaches at the confocal light and ultrastructural levels. Results Oxygen-glucose deprivation produced action potential failure and focal breakdown of the axolemma of small premyelinated axons at sites of contact with oligodendrocyte processes, which were also disrupted. The resulting axon loss was Ca2+ -dependent, Na+ - and Cl, -independent, and required activation of N -methyl-D-aspartic acid (NMDA) and non-NMDA GluRs. NMDA receptor expression was localized to oligodendrocyte processes at sites of contact with premyelinated axons, in addition to expression within compact myelin. No periaxonal NMDA receptor expression was observed on oligodendrocyte processes ensheathing large premyelinated axons and no protective effect of GluR block was observed in these axons. Interpretation NMDA receptor-mediated injury to oligodendrocyte processes navigating along small premyelinated axons precedes damage to the underlying axon, a phenomena that is lost following radial expansion and subsequent oligodendrocyte ensheathment. Ann Neurol 2009;66:682,693 [source] Experimental ocular acute hypertension-induced chromatinic alterations in astrocytic cells in rat optic nerveACTA OPHTHALMOLOGICA, Issue S232 2000N. Pescosolido Summary The effects of ocular acute hypertension experimentally induced on the astrocyte cells of rat have been studied. Evaluation was made of the damage to the chromatin of those cells by means of cytochemical (haematoxylin-eosin) analysis and of the state of fragmentation of the DNA by means of the TUNEL technique as well as the protective effect of the peroxide scavenger, troxol, on those events. [source] |