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Selective stimulation of astrocyte calcium in situ does not affect neuronal excitatory synaptic activity.

Neuron | May 24, 2007

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.

Pubmed ID: 17521573 RIS Download

Mesh terms: Animals | Animals, Newborn | Astrocytes | Calcium | Cell Communication | Drug Interactions | Excitatory Postsynaptic Potentials | GTP-Binding Protein alpha Subunits, Gq-G11 | Green Fluorescent Proteins | Hippocampus | In Vitro Techniques | Mice | Mice, Inbred C57BL | Mice, Transgenic | Neurotransmitter Agents | Oligopeptides | Patch-Clamp Techniques | Phosphopyruvate Hydratase | Presynaptic Terminals | Pyramidal Cells | Receptors, G-Protein-Coupled | Synapses | Synaptic Transmission