Astroglial calcium signaling displays short-term plasticity and adjusts synaptic efficacy

被引:22
|
作者
Sibille, Jeremie [1 ,2 ]
Zapata, Jonathan [1 ]
Teillon, Jeremie [1 ]
Rouach, Nathalie [1 ]
机构
[1] Coll France, CNRS UMR 7241, INSERM U1050, Ctr Interdisciplinary Res Biol,Neurol Interact Ce, F-75005 Paris, France
[2] Univ Paris Diderot, Sorbonne Paris Cite, Paris, France
来源
关键词
hippocampus; glia; neurons; neuroglial interactions; calcium signals; synapses; synaptic transmission; short-term plasticity; POTASSIUM CLEARANCE; EXTRACELLULAR K+; IN-VIVO; ASTROCYTES; POTENTIATION; NEURON; CURRENTS; RELEASE; OSCILLATIONS; STIMULATION;
D O I
10.3389/fncel.2015.00189
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Astrocytes are dynamic signaling brain elements able to sense neuronal inputs and to respond by complex calcium signals, which are thought to represent their excitability. Such signaling has been proposed to modulate, or not, neuronal activities ranging from basal synaptic transmission to epileptiform discharges. However, whether calcium signaling in astrocytes exhibits activity-dependent changes and acutely modulates shortterm synaptic plasticity is currently unclear. We here show, using dual recordings of astroglial calcium signals and synaptic transmission, that calcium signaling in astrocytes displays, concomitantly to excitatory synapses, short-term plasticity in response to prolonged repetitive and tetanic stimulations of Schaffer collaterals. We also found that acute inhibition of calcium signaling in astrocytes by intracellular calcium chelation rapidly potentiates excitatory synaptic transmission and short-term plasticity of Shaffer collateral CA1 synapses, i.e., paired-pulse facilitation and responses to tetanic and prolonged repetitive stimulation. These data reveal that calcium signaling of astrocytes is plastic and down-regulates basal transmission and short-term plasticity of hippocampal CA1 glutamatergic synapses.
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页数:10
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