Molecular Pathophysiology of White Matter Anoxic-Ischemic Injury

Ranson, Bruce R.; Acharya, Aninda B.; Goldberg, Mark P.

doi:10.1016/b0-44-306600-0/50051-1

Cited by 11 publications

(14 citation statements)

References 99 publications

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“…This is unfortunate because WM also suffers from glucose deprivation and damage to this region contributes to clinical deficits, which is not surprising, as WM represents a major portion (about 55%) of human forebrain volume . Moreover, the mechanisms of WM injury are distinctive compared to GM (see below). Finally, recent clinical reports show that WM can be selectively and severely injured by hypoglycemia .…”

Section: Discussionmentioning

confidence: 99%

Novel hypoglycemic injury mechanism: N‐methyl‐D‐aspartate receptor–mediated white matter damage

Yang

Hamner

Brown

et al. 2014

Annals of Neurology

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A note on versions:The version presented here may differ from the published version or from the version of record. If you wish to cite this item you are advised to consult the publisher's version. Please see the repository url above for details on accessing the published version and note that access may require a subscription. Aglycemia was produced by switching to 0 glucose ACSF. Supra-maximal compound action potentials (CAPs) were elicited using suction electrodes and axon function was quantified as the area under the CAP. Amino acid release was measured using HPLC. Extracellular [lactate] was measured using an enzyme electrode.Results: About 50% of MON axons were injured after 60 min of aglycemia (90%

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Section: Discussionmentioning

confidence: 99%

Novel hypoglycemic injury mechanism: N‐methyl‐D‐aspartate receptor–mediated white matter damage

Yang

Hamner

Brown

et al. 2014

Annals of Neurology

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“…In human focal ischemia, infarcts often involve the white matter (Ransom et al, 2004), and thorough examination of cellular injury in white matter is critical in animal stroke models. Previous studies investigating ischemic white matter injury in vivo assessed injury based on relative changes in expression of oligodendrocyte- and myelin-specific markers (see Ness et al, 2005 for review), but these epitopes may be transiently lost or masked under pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

Oligodendrocyte degeneration and recovery after focal cerebral ischemia

et al. 2010

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The vulnerability of oligodendrocytes to ischemic injury may contribute to functional loss in diseases of central white matter. Immunocytochemical methods to identify oligodendrocyte injury in experimental models rely on epitope availability, and fail to discriminate structural changes in oligodendrocyte morphology. We previously described the use of a lentiviral vector (LV) carrying eGFP under the myelin basic protein (MBP) promoter for selective visualization of oligodendrocyte cell bodies and processes. In this study, we used LV-MBP-eGFP to label oligodendrocytes in rat cerebral white matter prior to transient focal cerebral ischemia, and examined oligodendrocyte injury 24 hours, 48 hours and one week post-reperfusion by quantifying cell survival and assaying the integrity of myelin processes. There was progressive loss of GFP+ oligodendrocytes in ischemic white matter at 24 and 48 hrs. Surviving GFP+ cells had non-pyknotic nuclear morphology and were TUNEL-negative, but there was marked fragmentation of myelin processes as early as 24 hours after stroke. One week after stroke, we observed a restoration of GFP+ oligodendrocytes in ischemic white matter, reflected both by cell counts and by structural integrity of myelin processes. Proliferating cells were not the main source of GFP+ oligodendrocytes, as revealed by BrdU incorporation. These observations identify novel transient structural changes in oligodendrocyte cell bodies and myelinating processes, which may have consequences for white matter function after stroke.

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“…channel function (Chen et al 2002(Chen et al , 2004) and central nervous system regeneration (Cho et al 2005;Sugioka et al 1995). The rodent ON is considered to be an ideal model system because it is minimally disturbed during dissection (corpus callosum or dorsal columns of spinal cord are liable to injury during dissection and slicing) and, as it is an exclusively white matter tract, it is devoid of the complications of neuronal cell bodies, the retinal ganglion cells or glutamatergic synapses (Ransom et al 1997). Structurally, the adult tissue is relatively simple, being composed of myelinated axons, oligodendrocytes and astrocytes.…”

Section: Introductionmentioning

confidence: 99%

Morphological and electrophysiological characterization of the adult Siberian hamster optic nerve

et al. 2010

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Electrophysiological recordings and transmission electron microscopy were used to characterize the compound action potential (CAP) and morphology, respectively, of the optic nerve in the Siberian hamster. The CAP was polyphasic in nature, comprising four separate but overlapping peaks, thereby implying that four sub-populations of axons defined by conduction velocity are present in the nerve. The histological analysis of nerves from four animals revealed a cross-sectional area of 128,171 μm(2) containing 78,109 axons. All of the axons were myelinated, and measurements of axon surface area revealed values ranging from 0.09 to 9.92 μm(2), although 68.3% were <1 μm(2). In the regions of the nerve sampled, the area occupied by axons varied from 10.2 to 80.1%, but in 72.5% of these regions the axons occupied between 50 and 70% of the total cross-sectional area. All regions of the nerve expressed small axons, but larger axons (>2.5 μm(2)) were selectively distributed throughout the nerve. We conclude that the CAP recorded from hamster optic nerve displays four distinct peaks; however, morphological analysis failed to reveal a similar distribution of axon sizes.

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Molecular Pathophysiology of White Matter Anoxic-Ischemic Injury

Cited by 11 publications

References 99 publications

Novel hypoglycemic injury mechanism: N‐methyl‐D‐aspartate receptor–mediated white matter damage

Novel hypoglycemic injury mechanism: N‐methyl‐D‐aspartate receptor–mediated white matter damage

Oligodendrocyte degeneration and recovery after focal cerebral ischemia

Morphological and electrophysiological characterization of the adult Siberian hamster optic nerve

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