ArticleNeurochemical research2008
Potentiation by thrombin of hyposmotic glutamate and taurine efflux from cultured astrocytes: signalling chains.
Article in Neurochemical research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 5 citations in OpenAlex.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of protein-activated receptor (PAR-1) by thrombin potentiates the hyposmotic efflux of (3)H-D-aspartate and (3)H-taurine from cultured cerebellar astrocytes. This effect is mediated by a thrombin-elicited increase in cytosolic Ca(2+) levels [Ca(2+)](i) and the activation of phosphoinositide-3-kinase (PI3K). These signalling pathways operate independently showing additive effects if prevented simultaneously. The contribution of the Ca(2+)-mediated pathway to thrombin-increased D-aspartate or taurine efflux, evaluated by the inhibitory effect of preventing [Ca(2+)](i) rise, was higher for D-aspartate (64% efflux decrease) than for taurine (40% decrease). The PI3K blocker decreased 48% and 36% D-aspartate and taurine efflux, respectively. Hyposmolarity increases phosphorylation of EGFR and c-src, but thrombin did not enhance this effect. Blockade of EGFR/src phosphorylation marginally reduced (11-14%) the hyposmolarity plus thrombin efflux of D-aspartate; taurine efflux was more sensitive to these blockers (18-26%). Since thrombin has no effect increasing EGFR/src phosphorylation in astrocytes, the contribution of this transactivation pathway may represent the inhibition of the hyposmotic efflux solely.
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Registered trials
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