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We investigated the effect of diazoxide on neuronal survival in primary cultures of rat cortical neurons against oxygen-glucose deprivation (OGD). Diazoxide pre-treatment induced delayed pre-conditioning and almost entirely attenuated the OGD-induced neuronal death. Diazoxide inhibited succinate dehydrogenase and induced mitochondrial depolarization, free(More)
BMS-191095, reportedly a selective mitoK(ATP) channel opener which is free from the known side effects of the prototype mitoK(ATP) channel opener diazoxide, induced acute and delayed preconditioning against glutamate excitotoxicity and delayed preconditioning against oxygen-glucose deprivation in primary cultures of rat cortical neurons. BMS-191095 dose(More)
Uridine, like adenosine, is released under sustained depolarization and it can inhibit hippocampal neuronal activity, suggesting that uridine may be released during seizures and can be involved in epileptic mechanisms. In an in vivo microdialysis study, we measured the extracellular changes of nucleoside and amino acid levels and recorded cortical EEG(More)
Crude striatum synaptosomes (P2 fraction) from Fischer 344 female rats were incubated in the presence of ADP-chelated Fe3 (0.5-50 microM) and ascorbate (250 microM). Intrasynaptosomal conversion of tyrosine to dopamine (DA) was measured by 14CO2 evolution from L-[1-14C]tyrosine in the absence of added cofactors and DOPA decarboxylase. Malondialdehyde (MDA)(More)
We examined the effects of diazoxide, the putative mitochondrial adenosine triphosphate-sensitive potassium (mitoK(ATP)) channel opener, against glutamate excitotoxicity in primary cultures of rat cortical neurons. Cells were treated with diazoxide for 24 hr and then exposed to 200 microM glutamate. Cell viability was measured 24 hr after glutamate(More)
Diazoxide (DIAZ), an opener of mitochondrial ATP-sensitive K(+) channels (mK(ATP)), protects neurons against hypoxic/ischemic stress in vivo, however, direct evidence showing mitochondrial effects of DIAZ in postischemic neurons is lacking. We investigated if DIAZ affects mitochondrial alterations after global ischemia/reperfusion (I/R) in CA1 pyramidal(More)
Membrane lipids of brain synaptosomes of 2, 12 and 24 months old rats were labeled by stearic acid spin probes with a doxyl group in the C-5 and C-16 position, respectively. We demonstrated that the hydrophobic region of synaptosomal membranes became more rigid during the life span studied, and the region located nearer the surface of membranes displays a(More)
Indolicidin, a cationic antimicrobial tridecapeptide amide, is rich in proline and tryptophan residues. Its biological activity is intensively studied, but the details how indolicidin interacts with membranes are not fully understood yet. We report here an in situ atomic force microscopic study describing the effect of indolicidin on an artificial supported(More)
The excitatory amino acid glutamate is a potent vasodilator in the central nervous system. Glutamate-induced vasodilation is mediated primarily by N-methyl-D-aspartate (NMDA) and AMPA/kainate (KAIN) receptors. We have now tested whether two metabolites of the kynurenine pathway of tryptophan degradation acting at the NMDA receptor, the antagonist kynurenic(More)
Kynurenic acid (KYNA), a neuroactive metabolite of tryptophan that acts on different receptors (e.g. those of N-methyl-D-aspartate (NMDA) and presynaptic α7 nicotinic acetylcholine (nACh)), exerts fundamentally antiglutamatergic effects. In view of its antiglutamatergic properties, an elevation of the KYNA level within the brain might result in(More)