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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 92 (2005), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Susceptibility to audiogenic seizures, which are reflex seizures provoked by loud noise, can be induced in rodents by acoustic priming (exposing animals to strong auditory stimuli at an early developmental stage). Some strains of mice and rats are susceptible to audiogenic seizures without priming and these have been used as good experimental models with which to study epilepsies. Here we identified Vlgr1d and Vlgr1e, novel alternatively-spliced variants of Vlgr1b/MGR1, which, upon sequence analysis, were shown to be transcripts from a locus previously characterized as mass1. Vlgr1 (Vlgr1b, Vlgr1d and Vlgr1e) mRNA is expressed predominantly in the neuroepithelium of the developing mouse brain. Our protein-tagged experiment suggested that Vlgr1d and Vlgr1e are secretory molecules, while Vlgr1b is a receptor. Knockout mice lacking exons 2–4 of Vlgr1 were susceptible to audiogenic seizures without priming, although there were no apparent histological abnormalities in their brains. Ninety-five percent of these knockout mice exhibited wild running, a feature typical of the preconvulsive phase of audiogenic seizures triggered by loud noise (11 kHz, 105 dB), and 68% exhibited tonic convulsions at 3 weeks after birth. Our monogenic mice, which have a unique genetic background, serve as a useful tool for further studies on seizures.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-702X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  · Background: Diabetic keratopathy, frequently observed after vitreous surgery, has been thought to be related to the aldose reductase-catalyzed reaction. However, few reports have been published on the chronological changes in polyol accumulation and the effect of the aldose reductase inhibitor in the corneal epithelium or endothelium of galactosemic rats. Consequently, the polyol accumulation in corneal epithelium and endothelium with stroma of 50% galactose-fed rats and the preventive effect of an aldose reductase inhibitor, SNK-860, were biochemically analyzed. · Methods: Four-week-old male Sprague-Dawley rats were fed a 50% galactose diet without supplement or supplemented with a low (3 mg/kg b.w.) or high (30 mg/kg b.w.) dose of SNK-860 (Sanwa Kagaku Kenkyusho, Japan), or a normal diet. Polyol contents in the corneal epithelium or endothelium with stroma were individually measured using gas-liquid chromatography. · Results: Polyol in corneal epithelia accumulated quickly in the 1st week, reached a maximum at the 3rd week of feeding and then gradually decreased. Low- and high-dose SNK-860 treatment significantly inhibited polyol accumulation in the epithelium and endothelium with stroma, respectively. Changing to the normal or SNK-860 supplemented diets significantly inhibited polyol accumulation. · Conclusion: This finding indicates that oral administration of a new aldose reductase inhibitor, SNK-860, or systematic treatment of diabetes may be effective in preventing polyol pathway-induced corneal damage by quickly reducing the polyol level.
    Type of Medium: Electronic Resource
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