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The enzyme activities and the protein levels of Cl(-)-ATPase and Na+/K(+)-ATPase were examined in Alzheimer's disease (AD) brains. Cl(-)-ATPase and Na+/K(+)-ATPase activities in AD brains (n = 13) were significantly lower than those in age-matched control brains (n = 12). In contrast, there was no significant difference in anion-insensitive Mg2(+)-ATPase(More)
Although gamma-aminobutyric acid (GABA)C receptor rho1, rho2 and rho3 subunits are reportedly expressed in pyramidal and granule cells in the hippocampus at various developmental stages, it is not clear whether these three rho subunits are coexpressed in a single neuron. To attempt to answer this question, we performed single-cell RT-PCR for rho subunits(More)
The effects of anxiolytic honokiol derivative, dihydrohonokiol-B (DHH-B), on amyloid beta protein (Abeta(25-35), 10 nM)-induced changes in Cl(-)-ATPase activity, intracellular Cl- concentration ([Cl-]i) and glutamate neurotoxicity were examined in cultured rat hippocampal neurons. DHH-B (10 ng/ml) recovered Abeta-induced decrease in neuronal Cl(-)-ATPase(More)
We showed immunohistochemically the localization of 5 alpha-reductase-containing cells in the rat brain, using a rabbit antibody generated against 5 alpha-reductase rat type 1. The antibody was produced by injecting the synthetic peptide corresponding to the amino acids 38-53 of 5 alpha-reductase rat type 1, conjugated to keyhole limpet hemocyanin with(More)
The effects of an anxiolytic honokiol derivative, dihydrohonokiol-B (DHH-B) [3'-(2-propenyl)-5-propyl-(1,1'-biphenyl)-2,4'-diaol], on ammonia-induced increases in the intracellular Cl(-) concentration ([Cl(-)](i)) were examined using primary cultured rat hippocampal neurons. DHH-B (1-100 ng/ml), but not an inactive isomer of honokiol, magnolol (100 ng/ml),(More)
In our previous reports using primary cultured rat hippocampal neurons, pathophysiological concentrations (< or =10 nM) of amyloid beta proteins (Abetas) showed neurotoxicity via a phosphatidylinositol metabolism disorder, and soybean-derived phosphatidylinositol protected the neurons against the Abeta's neurotoxicity. In the present study, such a(More)
We previously found that pathophysiological concentrations (< or = 10 nm) of an amyloid beta protein (Abeta25-35) reduced the plasma membrane phosphatidylinositol monophosphate level in cultured rat hippocampal neurons with a decrease in phosphatidylinositol 4-monophosphate-dependent Cl- -ATPase activity. As this suggested an inhibitory effect of Abeta25-35(More)
AIMS We previously reported that the neurotoxicity of amyloid beta protein (Abeta(1-42), 10 nM) was blocked by an Abeta-derived tripeptide, Abeta(32-34) (Ile-Gly-Leu, IGL), suggesting that IGL may be a lead compound in the design of Abeta antagonists. In the present study, three stable forms of IGL peptide with acetylation of its N-terminal and/or amidation(More)
We previously reported that the neurotoxicity of pathophysiological concentrations of amyloid beta proteins (Abetas, 0.1-10nM) as assessed by the inhibition of type II phosphatidylinositol 4-kinase (PI4KII) activity and the enhancement of glutamate toxicity was blocked by a short fragment of Abeta, Abeta(31-35). Such protective effects of shorter fragments(More)
To test whether the increased intracellular Cl- concentration ([Cl-]i) is responsible for the enhanced glutamate toxicity, antisense oligonucleotide of ClP55, a Cl- -ATPase/pump associated protein, was transfected in cultured rat hippocampal neurons. Neuronal [Cl-]i in the antisense oligonucleotide-transfected culture increased to a level 3- to 4-fold(More)