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  • 1
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Transgenic mice expressing a mutated (G93A) human Cu/Znsuperoxide dismutase (SOD1) develop motor neuron pathology and clinicalsymptoms similar to those seen in patients with amyotrophic lateral sclerosis.Loss of motor neurons is most prominent in lumbar, followed by cervical cordand then brainstem. No significant cell death has been reported in motorcortex. The integrity of the cortical glutamate reuptake systems was evaluatedusing intracerebral microdialysis and western immunoblot assays for theglutamate transporters GLT-1, GLAST, and EAAC1. The basal extracellular fluidlevels of aspartate, glutamate, glutamine, 3,4-dihydroxyphenylacetic acid, and5-hydroxyindole-3-acetic acid were evaluated by HPLC. The extraction fractionof L-[3H]glutamate, corrected with [14C]mannitol, wasalso evaluated. GLT-1, EAAC1, and GLAST protein levels were determined bysemiquantitative chemiluminescence immunoblot of proteins frommembrane-enriched fractions. The relative optical density of film wastranslated into relative protein level by comparison with a standard controlmouse. The SOD1 mutant mice demonstrated a significant (p 〈 0.05)increase in basal levels of extracellular aspartate and glutamate. Inaddition, when the glutamate extraction fraction was challenged with exogenousunlabeled glutamate (500 μM) by reversed microdialysis, the glutamate extraction fraction in the mutant SOD1 mice was decreased significantly from control levels. The SOD1 mutant mice demonstrated no difference in the cortical protein levels of the glutamate transporter subtypes. This study demonstrates that in areas of no visible pathology and no loss of glutamate transporter proteins, SOD1 mutant mice have elevated extracellular fluid aspartate and glutamate levels and a decreased capacity to clear glutamate from the extracellular space.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0362-2525
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The primate cochlear nuclear complex exhibits several characteristic morphological differences in the various primate families from Lorisidae through Hominidae. The most striking differences occur in the organization of the dorsal cochlear nucleus in which the laminar pattern becomes progressively obscured. Granule cells form an external granular layer as well as being intermixed within the molecular and pyramidal layers in slow lorises and squirrel and rhesus monkeys. Whereas a prominent external granular layer remains in chimpanzees, granule cells are scant in other portions of the nucleus. Human adults lack an external granular layer. A small number of granule cells occur but with inconstant distribution. Primates lack the linear array of pyramidal cells oriented perpendicularly to the epithelial surface as seen in cats.The granule cell layer exhibits similar regression in development of the human cochlear complex. The external granular layer is prominent in the fetus but rapidly decreases in size after birth. It achieves its adult form prior to 18 months. The data suggest that neuronal attrition, or programmed cell death, may be the major mechanism accounting for the alterations that occur in the human granule cell layer.Other differences in cytoarchitecture, within the great apes and humans, include decreases in the small and giant cell populations of the cochlear complex. These changes, in consort with the organizational changes and reduction of granule cells as noted above, suggest a trend towards reduced intranuclear integration at the level of the cochlear nucleus coupled with encephalization of the auditory system.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The hereditary spastic paraplegias (HSPs; Strümpell-Lorrain syndrome, MIM number 18260) are a diverse class of disorders characterized by insidiously progressive lower-extremity spastic weakness (reviewed in refs. 1–3). Eight autosomal dominant HSP (ADHSP) loci have been identified, the ...
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