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Updated: May 17, 2026
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Dual Electrophysiological Recordings of Synaptically-evoked Astroglial and Neuronal Responses in Acute Hippocampal Slices
Published on: November 26, 2012
Heterosynaptic long-term depression mediated by ATP released from astrocytes
Jiadong Chen1, Zhibing Tan, Li Zeng
1Institute of Neuroscience and Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Glia
|October 10, 2012
Summary
Astrocytes release ATP to induce heterosynaptic long-term depression (hLTD), sharpening synaptic potentiation. This astrocyte-mediated mechanism is crucial for neural circuit plasticity.
Area of Science:
- Neuroscience
- Cell Biology
- Synaptic Plasticity
Background:
- Heterosynaptic long-term depression (hLTD) refines synaptic potentiation but its mechanism is unknown.
- Astrocytes are increasingly recognized for their role in synaptic function.
Purpose of the Study:
- To elucidate the mechanism of hLTD in the hippocampal CA1 region.
- To determine the role of astrocytes in activity-dependent synaptic plasticity.
Main Methods:
- Utilized channelrhodopsin-2 to selectively stimulate astrocytes in hippocampal CA1.
- Measured synaptic transmission and plasticity.
- Investigated the role of astrocyte calcium (Ca2+), P2Y receptors, and N-methyl-D-aspartate receptors.
Main Results:
- Stimulation-induced ATP release from astrocytes caused hLTD at untetanized synapses.
- Astrocyte Ca2+ elevation and P2Y receptor activation were necessary for hLTD.
- Blocking P2Y receptors or buffering astrocyte Ca2+ prevented hLTD without affecting LTP.
- Astrocytes were sufficient to mediate hLTD.
Conclusions:
- Astrocyte activation is necessary and sufficient for mediating hLTD.
- ATP release from astrocytes plays a key role in synaptic plasticity.
- Astrocytes actively participate in regulating neural circuit activity-dependent synaptic plasticity.
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