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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
PubMed

Insights

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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