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Related Experiment Video

Updated: Jan 9, 2026

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Astrocytic PERK Deficiency Drives Prefrontal Circuit Dysfunction and Depressive-Like Behaviors.

Kai Chen1, Riya Gupta2, Yosuke M Morizawa1

  • 1Department of Anesthesiology, Columbia University Irving Medical Center, New York, NY, 10032, USA.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
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Summary
This summary is machine-generated.

Reduced PERK in brain astrocytes contributes to depression. Restoring TSP1 in astrocytes may offer a new therapeutic strategy for major depressive disorder (MDD).

Keywords:
Nrf2PERKTSP1astrocytedepressiongene therapyprefrontal cortexsynaptic plasticity

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Area of Science:

  • Neuroscience
  • Cellular Biology
  • Glial Biology

Background:

  • Major depressive disorder (MDD) involves prefrontal cortex (PFC) circuit dysfunction.
  • Glial mechanisms contributing to MDD remain largely unknown.

Purpose of the Study:

  • Investigate the role of endoplasmic reticulum (ER) stress sensor PERK in PFC astrocytes in MDD.
  • Identify glial mechanisms underlying PFC circuit abnormalities in depression.

Main Methods:

  • Assessed PERK expression in human MDD patients and mouse models.
  • Utilized astrocyte-specific PERK deletion in mice.
  • Examined PFC circuit pathology, neuronal activity, and functional connectivity.
  • Investigated downstream molecular mechanisms including Nrf2, Ca2+ dynamics, and thrombospondin-1 (TSP1) expression.
  • Employed adeno-associated virus to restore astrocytic TSP1.

Main Results:

  • PERK expression was reduced in PFC astrocytes of MDD individuals and chronic stress models.
  • Astrocyte-specific PERK deletion induced depressive-like behaviors and PFC circuit pathology.
  • PERK deficiency led to reduced Nrf2, altered Ca2+ dynamics, and decreased TSP1 in astrocytes.
  • Restoring astrocytic TSP1 reversed behavioral and circuit deficits.

Conclusions:

  • Astrocyte PERK deficiency is a sufficient cause of synaptic and network dysfunction in depression.
  • Augmenting astrocytic TSP1 presents a potential therapeutic avenue for MDD.