Selective stimulation of astrocyte calcium in situ does not affect neuronal excitatory synaptic activity |
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Authors: | Fiacco Todd A Agulhon Cendra Taves Sarah R Petravicz Jeremy Casper Kristen B Dong Xinzhong Chen Ju McCarthy Ken D |
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Affiliation: | Department of Pharmacology, 1004 Mary Ellen Jones Building CB# 7365, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7365, USA. |
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Abstract: | Astrocytes are considered the third component of the synapse, responding to neurotransmitter release from synaptic terminals and releasing gliotransmitters--including glutamate--in a Ca(2+)-dependent manner to affect neuronal synaptic activity. Many studies reporting astrocyte-driven neuronal activity have evoked astrocyte Ca(2+) increases by application of endogenous ligands that directly activate neuronal receptors, making astrocyte contribution to neuronal effect(s) difficult to determine. We have made transgenic mice that express a Gq-coupled receptor only in astrocytes to evoke astrocyte Ca(2+) increases using an agonist that does not bind endogenous receptors in brain. By recording from CA1 pyramidal cells in acute hippocampal slices from these mice, we demonstrate that widespread Ca(2+) elevations in 80%-90% of stratum radiatum astrocytes do not increase neuronal Ca(2+), produce neuronal slow inward currents, or affect excitatory synaptic activity. Our findings call into question the developing consensus that Ca(2+)-dependent glutamate release by astrocytes directly affects neuronal synaptic activity in situ. |
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