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A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons.
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Zeitschriftentitel: | Proceedings of the National Academy of Sciences |
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Personen und Körperschaften: | , |
In: | Proceedings of the National Academy of Sciences, 85, 1988, 22, S. 8737-8741 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Proceedings of the National Academy of Sciences
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Schlagwörter: |
author_facet |
Murphy, S N Miller, R J Murphy, S N Miller, R J |
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author |
Murphy, S N Miller, R J |
spellingShingle |
Murphy, S N Miller, R J Proceedings of the National Academy of Sciences A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. Multidisciplinary |
author_sort |
murphy, s n |
spelling |
Murphy, S N Miller, R J 0027-8424 1091-6490 Proceedings of the National Academy of Sciences Multidisciplinary http://dx.doi.org/10.1073/pnas.85.22.8737 <jats:p>We investigated the effect of various excitatory amino acids on intracellular free Ca2+ concentration ( [Ca2+]i) in single mouse hippocampal neurons in vitro by using the Ca2+-sensitive dye fura-2. In normal physiological solution, glutamate, kainate, N-methyl-D-aspartate, and quisqualate all produced increases in [Ca2+]i. When all extracellular Ca2+ was removed, kainate and N-methyl-D-aspartate were completely ineffective, but quisqualate and glutamate were able to produce a spike-like Ca2+ transient, presumably reflecting the release of Ca2+ from intracellular stores. Ca2+ transients of similar shape could also be produced by the alpha 1-adrenergic agonist phenylephrine. After the production of a Ca2+ transient a second addition of quisqualate was ineffective unless intracellular stores were refilled by loading the cell with Ca2+ following depolarization in Ca2+-containing medium. None of the conventional excitatory amino acid receptor antagonists inhibited the Ca2+-mobilizing effects of quisqualate. Furthermore alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) was unable to produce Ca2+ mobilization in Ca2+-free medium, although it could produce Ca2+ influx in Ca2+-containing medium. Thus, glutamate can produce mobilization of Ca2+ from intracellular stores in hippocampal neurons by acting on a quisqualate-sensitive but AMPA-insensitive receptor. This receptor is therefore distinct from the quisqualate receptor that produces cell depolarization. The possibility that this Ca2+-mobilizing effect is mediated by inositol triphosphate production is discussed.</jats:p> A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. Proceedings of the National Academy of Sciences |
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Proceedings of the National Academy of Sciences, 1988 |
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Proceedings of the National Academy of Sciences, 1988 |
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1988 |
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Proceedings of the National Academy of Sciences |
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title |
A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
title_unstemmed |
A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
title_full |
A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
title_fullStr |
A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
title_full_unstemmed |
A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
title_short |
A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
title_sort |
a glutamate receptor regulates ca2+ mobilization in hippocampal neurons. |
topic |
Multidisciplinary |
url |
http://dx.doi.org/10.1073/pnas.85.22.8737 |
publishDate |
1988 |
physical |
8737-8741 |
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<jats:p>We investigated the effect of various excitatory amino acids on intracellular free Ca2+ concentration ( [Ca2+]i) in single mouse hippocampal neurons in vitro by using the Ca2+-sensitive dye fura-2. In normal physiological solution, glutamate, kainate, N-methyl-D-aspartate, and quisqualate all produced increases in [Ca2+]i. When all extracellular Ca2+ was removed, kainate and N-methyl-D-aspartate were completely ineffective, but quisqualate and glutamate were able to produce a spike-like Ca2+ transient, presumably reflecting the release of Ca2+ from intracellular stores. Ca2+ transients of similar shape could also be produced by the alpha 1-adrenergic agonist phenylephrine. After the production of a Ca2+ transient a second addition of quisqualate was ineffective unless intracellular stores were refilled by loading the cell with Ca2+ following depolarization in Ca2+-containing medium. None of the conventional excitatory amino acid receptor antagonists inhibited the Ca2+-mobilizing effects of quisqualate. Furthermore alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) was unable to produce Ca2+ mobilization in Ca2+-free medium, although it could produce Ca2+ influx in Ca2+-containing medium. Thus, glutamate can produce mobilization of Ca2+ from intracellular stores in hippocampal neurons by acting on a quisqualate-sensitive but AMPA-insensitive receptor. This receptor is therefore distinct from the quisqualate receptor that produces cell depolarization. The possibility that this Ca2+-mobilizing effect is mediated by inositol triphosphate production is discussed.</jats:p> |
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author | Murphy, S N, Miller, R J |
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description | <jats:p>We investigated the effect of various excitatory amino acids on intracellular free Ca2+ concentration ( [Ca2+]i) in single mouse hippocampal neurons in vitro by using the Ca2+-sensitive dye fura-2. In normal physiological solution, glutamate, kainate, N-methyl-D-aspartate, and quisqualate all produced increases in [Ca2+]i. When all extracellular Ca2+ was removed, kainate and N-methyl-D-aspartate were completely ineffective, but quisqualate and glutamate were able to produce a spike-like Ca2+ transient, presumably reflecting the release of Ca2+ from intracellular stores. Ca2+ transients of similar shape could also be produced by the alpha 1-adrenergic agonist phenylephrine. After the production of a Ca2+ transient a second addition of quisqualate was ineffective unless intracellular stores were refilled by loading the cell with Ca2+ following depolarization in Ca2+-containing medium. None of the conventional excitatory amino acid receptor antagonists inhibited the Ca2+-mobilizing effects of quisqualate. Furthermore alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) was unable to produce Ca2+ mobilization in Ca2+-free medium, although it could produce Ca2+ influx in Ca2+-containing medium. Thus, glutamate can produce mobilization of Ca2+ from intracellular stores in hippocampal neurons by acting on a quisqualate-sensitive but AMPA-insensitive receptor. This receptor is therefore distinct from the quisqualate receptor that produces cell depolarization. The possibility that this Ca2+-mobilizing effect is mediated by inositol triphosphate production is discussed.</jats:p> |
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spelling | Murphy, S N Miller, R J 0027-8424 1091-6490 Proceedings of the National Academy of Sciences Multidisciplinary http://dx.doi.org/10.1073/pnas.85.22.8737 <jats:p>We investigated the effect of various excitatory amino acids on intracellular free Ca2+ concentration ( [Ca2+]i) in single mouse hippocampal neurons in vitro by using the Ca2+-sensitive dye fura-2. In normal physiological solution, glutamate, kainate, N-methyl-D-aspartate, and quisqualate all produced increases in [Ca2+]i. When all extracellular Ca2+ was removed, kainate and N-methyl-D-aspartate were completely ineffective, but quisqualate and glutamate were able to produce a spike-like Ca2+ transient, presumably reflecting the release of Ca2+ from intracellular stores. Ca2+ transients of similar shape could also be produced by the alpha 1-adrenergic agonist phenylephrine. After the production of a Ca2+ transient a second addition of quisqualate was ineffective unless intracellular stores were refilled by loading the cell with Ca2+ following depolarization in Ca2+-containing medium. None of the conventional excitatory amino acid receptor antagonists inhibited the Ca2+-mobilizing effects of quisqualate. Furthermore alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) was unable to produce Ca2+ mobilization in Ca2+-free medium, although it could produce Ca2+ influx in Ca2+-containing medium. Thus, glutamate can produce mobilization of Ca2+ from intracellular stores in hippocampal neurons by acting on a quisqualate-sensitive but AMPA-insensitive receptor. This receptor is therefore distinct from the quisqualate receptor that produces cell depolarization. The possibility that this Ca2+-mobilizing effect is mediated by inositol triphosphate production is discussed.</jats:p> A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. Proceedings of the National Academy of Sciences |
spellingShingle | Murphy, S N, Miller, R J, Proceedings of the National Academy of Sciences, A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons., Multidisciplinary |
title | A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
title_full | A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
title_fullStr | A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
title_full_unstemmed | A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
title_short | A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
title_sort | a glutamate receptor regulates ca2+ mobilization in hippocampal neurons. |
title_unstemmed | A glutamate receptor regulates Ca2+ mobilization in hippocampal neurons. |
topic | Multidisciplinary |
url | http://dx.doi.org/10.1073/pnas.85.22.8737 |