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Modulation of the glutamate-evoked release of arachidonic acid from mouse cortical neurons: involvement of a pH-sensitive membrane phospholipase A2

N Stella, L Pellerin and PJ Magistretti
Journal of Neuroscience 1 May 1995, 15 (5) 3307-3317; DOI: https://doi.org/10.1523/JNEUROSCI.15-05-03307.1995
N Stella
Laboratoire de Recherches Neurologiques, Faculte de Medecine, Universite de Lausanne, Switzerland.
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L Pellerin
Laboratoire de Recherches Neurologiques, Faculte de Medecine, Universite de Lausanne, Switzerland.
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PJ Magistretti
Laboratoire de Recherches Neurologiques, Faculte de Medecine, Universite de Lausanne, Switzerland.
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Abstract

Excitatory synaptic transmission is associated with changes in both extracellular and intracellular pH. Using mouse cortical neurons in primary cultures, we studied the sensitivity of glutamate-evoked release of 3H-arachidonic acid (3H-AA) to changes in extracellular pH (pHo) and related intracellular pH (pHi). As pHo was shifted from 7.2 to 7.8, the glutamate-evoked release of 3H-AA was enhanced by approximately threefold. The effect of alkaline pHo on the glutamate response was rapid, becoming significant within 2 min. 3H-AA release, evoked by both NMDA and kainate, was also enhanced by pHo alkalinization. NMDA- and kainate-induced increase in free intracellular Ca2+ was unaffected by changing pHo from 7.2 to 7.8, indicating that the receptor-induced Ca2+ influx is not responsible for the pHo sensitivity of the glutamate-evoked release of 3H-AA. Alkalinization of pHi obtained by incubating neurons in the presence of HCO3- or NH4 enhanced the glutamate-evoked release of 3H-AA, while pHi acidification obtained by blockade of Na+/H+ and Cl-/HCO3- exchangers decreased the glutamate response. Membrane-bound phospholipase A2 (mPLA2) activity was stimulated by Ca2+ in a pH-dependent manner, increasing its activity as pH was shifted from 7.2 to 7.8. This pH profile corresponds to the pH profile of the glutamate-, NMDA- and kainate-evoked release of 3H-AA. Taken together, these results indicate that the glutamate-evoked release of 3H-AA may be mediated by the pH- sensitive mPLA2. Since excitatory neurotransmission mediated by glutamate results in both pHo and pHi changes and since AA enhances glutamatergic neurotransmission at both pre- and postsynaptic levels, the data reported here reveals a possible molecular mechanism whereby glutamate can modulate its own signalling efficacy in a pH-dependent manner by regulating the release of AA.

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The Journal of Neuroscience: 15 (5)
Journal of Neuroscience
Vol. 15, Issue 5
1 May 1995
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Modulation of the glutamate-evoked release of arachidonic acid from mouse cortical neurons: involvement of a pH-sensitive membrane phospholipase A2
N Stella, L Pellerin, PJ Magistretti
Journal of Neuroscience 1 May 1995, 15 (5) 3307-3317; DOI: 10.1523/JNEUROSCI.15-05-03307.1995

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Modulation of the glutamate-evoked release of arachidonic acid from mouse cortical neurons: involvement of a pH-sensitive membrane phospholipase A2
N Stella, L Pellerin, PJ Magistretti
Journal of Neuroscience 1 May 1995, 15 (5) 3307-3317; DOI: 10.1523/JNEUROSCI.15-05-03307.1995
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