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Biphasic enhacement of nitric oxide synthase activity and cGMP level following brain ischemia in gerbils

100%
Strosznajder J., Chalimoniuk M.
Acta Neurobiologiae Experimentalis
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1996
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vol. 56
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issue 1
71-81
EN
This study was aimed to examine properties and changes in nitric oxide synthase (NOS) activity and cGMP level during reperfusion after 5 min of brain ischemia in gerbils. Animals were treated 5 min befor ischemia with NOS inhibitors: N-nitro-L-arginine (NNLA), or 7-Nitroindazole (7-NI), or with the inhibitor of guanylate cyclase, LY 83583, or with hydrocortisone for 7 days before ischemia. Northern bolt analysis was performed using specific cDNA for inducible NOS. It was observed that ischemia significantly enhances NOS activity and cGMP level. During reperfusion, biphasic increase in NOS activity and cGMP level took place with two peaks 15 min and 2 h after ischemia. NNLA, 7-NI, and LY 83583 eliminated enhancements of NOS activity and cGMP level, whereas glucocorticoid remained without effect. There was no activation of gene encoding inducible NOS (iNOS). Our results indicate that ischemia-reperfusion activates constitutive NOS. It is suggested that nitric oxide (NO) production during reperfusion is related to neuronal degeneration and that inhibitor of NOS offers a new therapeutical strategies.
2
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Ischemia-related alteration of GABAA-operated chloride channel properties in gerbil hippocampus and cerebral cortex

81%
Strosznajder J., Koladkiewicz I., Chalimoniuk M., Samochocki M.
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issue 2
95-102
EN
The properties of GABA-gated chloride (Cl^-) channels in ischemia-reperfusion injury were studied by determination of the binding and dissociation kinetics of a specific Cl^- channel ligand, tert-butylbicyclophosphoro[^35S]thionate (TBPS) and by determination of ^36Cl^- uptake in the presence of the GABAA receptor agonist, muscimol. Four days after ischemia a small but insignificant decrease of [^35S]TBPS binding to synaptic plasma membranes (SPM) was observed in the hippocampus and cerebral cortex as compared to control. The effect of ischemia was larger and statistically significant after the first and second month of reperfusion, constituting 20% inhibition of [^35S]TBPS binding to SPM of sham-operated gerbils. On the other hand, the half-life of fast phase [^35S]TBPS dissociation four days after ischemia was markedly diminished by about 40%-50% as compared to its control value and persisted during the first and second month of reperfusion in the hippocampal SPM. A similar but less potent reduction of the half-life of the fast phase of [^35S]TBPS dissociation (about 30% versus control) appeared one and two months after ischemia in cerebral cortex SPM. One month after ischemia muscimol-stimulated ^36Cl^- uptake into cerebral cortex synaptoneurosomes was lowered as compared with control uptake, but remained statistically insignificant in the whole range of muscimol concentrations tested. Our results indicated that ischemia-reperfusion injury significantly decreases opening time of GABAA receptor-gated Cl^- channels in the hippocampus and cerebral cortex, which may lower the hyperpolarization ability of this receptor complex leading to an imbalance between excitatory and inhibitory neurotransmitter pathways in these brain areas, and in consequence to neuronal dysfunction or degeneration.
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