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Biomedical subjects

N Oguro

Publications and source records attributed to N Oguro.

9 recordsLinked to original sources
PubMed2001

Global ischemia-induced increases in the gap junctional proteins connexin 32 (Cx32) and Cx36 in hippocampus and enhanced vulnerability of Cx32 knock-out mice.

Gap junctions are conductive channels that connect the interiors of coupled cells. In the hippocampus, GABA-containing hippocampal interneurons are interconnected by gap junctions, which mediate electrical coupling and synchronous firing and thereby promote inhibitory transmission. The present study was undertaken to examine the hypothesis that the gap junctional proteins connexin 32 (Cx32; expressed by oligodendrocytes, interneurons, or both), Cx36 (expressed by interneurons), and Cx43 (expressed by astrocytes) play a role in defining cell-specific patterns of neuronal death in hippocampus after global ischemia in mice. Global ischemia did not significantly alter Cx32 and Cx36 mRNA expression and slightly increased Cx43 mRNA expression in the vulnerable CA1, as assessed by Northern blot analysis and in situ hybridization. Global ischemia induced a selective increase in Cx32 and Cx36 but not Cx43 protein abundance in CA1 before onset of neuronal death, as assessed by Western blot analysis. The increase in Cx32 and Cx36 expression was intense and specific to parvalbumin-positive inhibitory interneurons of CA1, as assessed by double immunofluorescence. Protein abundance was unchanged in CA3 and dentate gyrus. The finding of increase in connexin protein without increase in mRNA suggests regulation of Cx32 and Cx36 expression at the translational or post-translational level. Cx32(Y/-) null mice exhibited enhanced vulnerability to brief ischemic insults, consistent with a role for Cx32 gap junctions in neuronal survival. These findings suggest that Cx32 and Cx36 gap junctions may contribute to the survival and resistance of GABAergic interneurons, thereby defining cell-specific patterns of global ischemia-induced neuronal death.

Animals↗
PubMed1999

Knockdown of AMPA receptor GluR2 expression causes delayed neurodegeneration and increases damage by sublethal ischemia in hippocampal CA1 and CA3 neurons.

Considerable evidence suggests that Ca(2+)-permeable AMPA receptors are critical mediators of the delayed, selective neuronal death associated with transient global ischemia and sustained seizures. Global ischemia suppresses mRNA and protein expression of the glutamate receptor subunit GluR2 and increases AMPA receptor-mediated Ca(2+) influx into vulnerable neurons of the hippocampal CA1 before the onset of neurodegeneration. Status epilepticus suppresses GluR2 mRNA and protein in CA3 before neurodegeneration in this region. To examine whether acute downregulation of the GluR2 subunit, even in the absence of a neurological insult, can cause neuronal cell death, we performed GluR2 "knockdown" experiments. Intracerebral injection of antisense oligodeoxynucleotides targeted to GluR2 mRNA induced delayed death of pyramidal neurons in CA1 and CA3. Antisense-induced neurodegeneration was preceded by a reduction in GluR2 mRNA, as indicated by in situ hybridization, and in GluR2 protein, as indicated by Western blot analysis. GluR2 antisense suppressed GluR2 mRNA in the dentate gyrus but did not cause cell death. The AMPA receptor antagonist 6-cyano-7-nitroquinoxiline-2,3-dione (CNQX) and the Ca(2+)-permeable AMPA receptor channel blocker 1-naphthyl acetyl spermine protected against antisense-induced cell death. This result indicates that antisense-induced cell death is mediated by Ca(2+)-permeable AMPA receptors. GluR2 antisense and brief sublethal global ischemia acted synergistically to cause degeneration of pyramidal neurons, consistent with action by a common mechanism. These findings demonstrate that downregulation of GluR2 is sufficient to induce delayed death of specific neuronal populations.

Animals↗
PubMed1990

Multi-institutional survey of the Rett syndrome in Japan.

The results of the first multi-institutional survey of the Rett syndrome in Japan are reported. The survey was performed during 1985 and 1986. Eighty-nine cases were collected, of which 54 cases were confirmed to have the Rett syndrome. The ages of the patients ranged between 1 and 26 years. The clinical onsets occurred after 18 months of age in 28 cases, and before the age of one year in 26. No familial cases nor consanguinity was found. The incidence of perinatal abnormalities among the patients was not significantly higher than in other diseases in which no perinatal factors are involved.

Adult↗
PubMed1989

Tricho-rhino-phalangeal syndrome type I with severe mental retardation due to interstitial deletion of 8q23.3-24.13.

Here we report on a 13-year-old boy who had an interstitial deletion of the long arm of chromosome 8 [46,XY,del(8)(pter----q23.3::q24.13----qter)]. He had the facial features of the tricho-rhino-phalangeal (TRP) syndrome and severe mental retardation, but lacked multiple exostoses. This is the first report with such a peculiar combination of abnormalities and interstitial deletion of 8q.

Chromosome Banding↗
PubMed1989

Prometaphase chromosomes in the tricho-rhino-phalangeal syndrome type I.

Prometaphase chromosome analysis was undertaken in a patient with familial tricho-rhino-phalangeal syndrome type I (TRPS-I). The patient had apparently normal chromosomes and produced counterevidence to part of Bühler's hypothesis. Thus, although some cases of typical TRPS-I may be derived from a deletion of 8q24.12, others might be caused by gene mutation or submicroscopic deletion involving the corresponding locus within the band 8q24.11----24.13.

Abnormalities, Multiple↗