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- W2290193694 abstract "The roles of protein kinase C (PKC) and Li+ in N-methyl-D-aspartate (NMDA)-evoked releases of adenosine and noradrenaline (NA) were studied. In the absence of Mg2+, activation of PKC by phorbol 12-myristate 13-acetate (PMA) potentiated the release of adenosine evoked by 20muM NMDA and the release of [3H]NA evoked by 100muM NMDA. The potentiating effects of PMA on NMDA-evoked releases of adenosine and NA were reversed by inhibition of PKC with GF109,203X (GFX). GFX by itself had no effect on NMDA-evoked release of either adenosine or NA, suggesting that endogenous PKC does not play a role in NMDA-evoked releases. Li+, at concentrations of 1.5mM or 10mM, potentiated 300muM NMDA-evoked release of NA but had no effect on the release of adenosine. In the presence of Mg2+, NMDA-evoked release of NA was essentially abolished, whereas adenosine release persisted. Under these conditions, PMA or Li+ did not permit NMDA-evoked release of NA to occur, nor did they increase NMDA-evoked adenosine release. Taken together, these results indicate that PKC does not play an essential role in NMDA-evoked release of either adenosine or NA. However, activation of PKC potentiates the release of adenosine and NA evoked by submaximal concentrations of NMDA, but not by relieving the voltage-sensitive Mg 2+ block of NMDA receptors." @default.
- W2290193694 created "2016-06-24" @default.
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- W2290193694 date "2000-01-01" @default.
- W2290193694 modified "2023-09-26" @default.
- W2290193694 title "Release of glutamate, noradrenaline and adenosine from rat parietal cortical slices." @default.
- W2290193694 hasPublicationYear "2000" @default.
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