Hippocampal short- and long-term plasticity are not modulated by astrocyte Ca2+ signaling
The concept that astrocytes release neuroactive molecules (gliotransmitters) to affect synaptic transmission has been a paradigm shift in neuroscience research over the past decade. This concept suggests that astrocytes, together with pre- and postsynaptic neuronal elements, make up a functional synapse. Astrocyte release of gliotransmitters (for example, glutamate and adenosine triphosphate) is generally accepted to be a Ca2+-dependent process. We used two mouse lines to either selectively increase or obliterate astrocytic Gq G protein-coupled receptor Ca2+ signaling to further test the hypothesis that astrocytes release gliotransmitters in a Ca2+-dependent manner to affect synaptic transmission. Neither increasing nor obliterating astrocytic Ca2+ fluxes affects spontaneous and evoked excitatory synaptic transmission or synaptic plasticity. Our findings suggest that, at least in the hippocampus, the mechanisms of gliotransmission need to be reconsidered.
Errataetall: |
CommentIn: Science. 2010 Mar 5;327(5970):1212-3. - PMID 20203041 |
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Medienart: |
E-Artikel |
Erscheinungsjahr: |
2010 |
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Erschienen: |
2010 |
Enthalten in: |
Zur Gesamtaufnahme - volume:327 |
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Enthalten in: |
Science (New York, N.Y.) - 327(2010), 5970 vom: 05. März, Seite 1250-4 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Agulhon, Cendra [VerfasserIn] |
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Links: |
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Anmerkungen: |
Date Completed 19.03.2010 Date Revised 16.03.2022 published: Print CommentIn: Science. 2010 Mar 5;327(5970):1212-3. - PMID 20203041 Citation Status MEDLINE |
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doi: |
10.1126/science.1184821 |
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funding: |
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PPN (Katalog-ID): |
NLM195542703 |
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520 | |a The concept that astrocytes release neuroactive molecules (gliotransmitters) to affect synaptic transmission has been a paradigm shift in neuroscience research over the past decade. This concept suggests that astrocytes, together with pre- and postsynaptic neuronal elements, make up a functional synapse. Astrocyte release of gliotransmitters (for example, glutamate and adenosine triphosphate) is generally accepted to be a Ca2+-dependent process. We used two mouse lines to either selectively increase or obliterate astrocytic Gq G protein-coupled receptor Ca2+ signaling to further test the hypothesis that astrocytes release gliotransmitters in a Ca2+-dependent manner to affect synaptic transmission. Neither increasing nor obliterating astrocytic Ca2+ fluxes affects spontaneous and evoked excitatory synaptic transmission or synaptic plasticity. Our findings suggest that, at least in the hippocampus, the mechanisms of gliotransmission need to be reconsidered | ||
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