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Related Experiment Videos

Cocaine Triggers Astrocyte-Mediated Synaptogenesis.

Junshi Wang1, King-Lun Li1, Avani Shukla2

  • 1Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania.

Biological Psychiatry
|October 18, 2020
PubMed
Summary

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This summary is machine-generated.

Cocaine use triggers astrocyte signaling to create silent synapses in the brain, which are crucial for drug memories and relapse. Blocking this pathway reduces cocaine seeking behavior.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Addiction Research

Background:

  • Synaptogenesis, the formation of new neural connections, is vital for brain development.
  • Astrocyte-derived thrombospondins (TSPs) and their neuronal receptor α2δ-1 mediate developmental synaptogenesis.
  • This study investigates if this mechanism is reactivated by cocaine in adult brains.

Purpose of the Study:

  • To determine if cocaine experience induces synaptogenesis and silent synapse formation in the adult nucleus accumbens shell (NAcSh).
  • To examine the role of astrocyte-thrombospondin-α2δ-1 signaling in cocaine-induced silent synapse generation.
  • To assess the behavioral impact of astrocyte-mediated synaptogenesis on cocaine seeking and relapse.

Main Methods:

  • Astrocyte calcium (Ca2+) imaging in mouse models.
Keywords:
AccumbensAstrocyteCocaineSilent synapseSynaptogenesisThrombospondin

Related Experiment Videos

  • Utilizing genetic mouse lines, viral-mediated gene transfer, and operant behavioral procedures.
  • Monitoring NAcSh astrocyte responses to cocaine administration and analyzing TSP-α2δ-1 signaling.

    • Main Results:

    • Cocaine administration increased NAcSh astrocyte Ca2+ events.
    • Inhibiting astrocytic Ca2+ blocked cocaine-induced silent synapse formation.
    • Genetic or pharmacological disruption of the TSP2-α2δ-1 pathway prevented silent synapse generation and reduced cocaine seeking behavior.

    Conclusions:

    • Astrocyte-mediated synaptogenesis generates silent synapses in response to cocaine.
    • These silent synapses store memory traces associated with drug cues.
    • This mechanism contributes significantly to cocaine relapse by reinforcing drug-associated memories.