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In vitro-evaluation of lipid emulsions as vehicles for the administration of xenon: Interaction with NMDA receptors

100%
Weigt H. U., Georgieff M., Fohr K. J., Adolph O.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 2
207-216
EN
The noble gas xenon is an antagonist of the NMDA (N-methyl-D-aspartate)-type glutamate receptor which may account for the ideal anesthetic profile and potent neuroprotective properties demonstrated even at subanesthetic concentrations. Because lipid emulsions also promote NMDA antagonistic effects they may serve as ideal carriers for xenon. In this in vitro study, we investigated the efficacy of xenon dissolved in various lipid emulsions (Intralipid?, Lipofundin?, ClinOleic? and Abbolipid?) on NMDA-evoked currents in cultured cortical neurons. The NMDA receptor blocking property at a clinically relevant concentration seen in the lipid emulsions tested may contribute to the anesthetic, analgetic and neuroprotective effects of xenon administered by way of these lipid carriers. Abbolipid? may serve as the most acceptable carrier since the NMDA antagonistic effect of xenon was enhanced in combination with this emulsion.
2
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NMDA receptors and nitric oxide regulate prostaglandin D2 synthesis in the rabbit hippocampus in vivo

100%
Lazarewicz J. W., Salinska S. E., Salinska E., Stafiej S. A., Stafiej A., Ziembowicz Z. A., Ziembowicz A., Zieminska Z. E., Zieminska E.
Acta Neurobiologiae Experimentalis
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2000
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vol. 60
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issue 4
427-435
EN
The aim of this in vivo microdialysis study was to characterise the regulation of prostaglandin D2 (PgD2) synthesis by NMDA receptors in the rabbit hippocampus in relation to changes in extracellular Ca2+ concentration ([Ca2+]e) and nitric oxide (NO) levels. Samples of dialysate were analysed for changes in PgD2 concentration, in [Ca2+]e and in the level of NO. The results demonstrated that a 20-min pulse application of 0.1 - 2.5 mM NMDA via a microdialysis probe induced a prolonged stimulation of PgD2 release that was sensitive to competitive NMDA receptor antagonists. An inhibitor of voltage-sensitive Na+ channels, tetrodotoxin, did not influence this effect but significantly suppressed basal PgD2 production, whereas a NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), prevented NMDA-evoked NO release and inhibited NMDA-induced PgD2 release in an L-arginine-sensitive manner. NO donors, S-nitroso-N-acetylpenicillamine and sodium nitroprusside, stimulated PgD2 release. NMDA-evoked decrease in [Ca2+]e was insensitive to TTX and L-NAME. These results demonstrate an in vivo NMDA receptor-mediated modulation of PgD2 synthesis in the brain, in which NO participates.
3
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Differential expression of NMDA-evoked 45Ca release in rat hippocampal regions in vivo

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Lazarewicz J., Rybkowski W.
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EN
Recently we detected NMDA-induced 45Ca release in the rat dentate gyrus in vivo, attributable to the Ca2+ release (CICR) from the endoplasmic reticulum via ryanodine channels.In these experiments we compare expression of NMDA-evoked 45Ca release in the rat dentate gyrus (DG), CA1 and subiculum (SUB).The release of 45Ca was studied using in vivo prelabelled hippocampal regions.It was shown thet NMDA-induced 45Ca release, highly pronounced in the rat DG/CA4, is significantly less expressed in the CA1, whereas in the SUB and NMDA-evoked decrease in 45Ca efflux was noted.This corresponds to distribution of ryanodine receptors in the rat hippocampus, known from the literature.Expression of NMDA-evoked 45Ca release in these rat hippocampal regions which are enriched in ryanodine receptors supports our working hypothesis that CICR via ryanodine channels may be mainly responsible for 45Ca release.
4
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Biphasic effect of the NMDA receptor antagonist MK 801 on the nocturnal NAT activity in chick retina

63%
Zawilska J. B., Rosiak J., Nowak J. Z., Jenek J.
Acta Neurobiologiae Experimentalis
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1997
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vol. 57
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issue 2
163
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