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Related Experiment Video

Updated: Jun 11, 2025

Strategies for Assessing Autistic-Like Behaviors in Mice
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Autophagy defects at weaning impair complement-dependent synaptic pruning and induce behavior deficits.

Xi Su1,2,3,4,5, Guanyu Wang6,7,8, Senqi Liu6,7,8

  • 1Henan Mental Hospital, The Second Affiliated Hospital of Xinxiang Medical University, 388 Middle Jianshe Road, Xinxiang, 453002, China. suxi198919@163.com.

Journal of Neuroinflammation
|September 28, 2024
PubMed
Summary
This summary is machine-generated.

Defective autophagy is linked to schizophrenia (SCZ). Activating autophagy early in life can reverse SCZ-related behavioral and synaptic deficits in a rat model.

Keywords:
AutophagyComplementMaternal immune activationSchizophreniaSynaptic pruning

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Area of Science:

  • Neuroscience
  • Genetics
  • Cell Biology

Background:

  • Autophagy is vital for synaptic plasticity and dendritic spine structure.
  • The specific role of autophagy in schizophrenia (SCZ) and its impact on synaptic function are not well understood.

Purpose of the Study:

  • To investigate the association between autophagy-related genes and SCZ.
  • To explore the mechanisms by which autophagy influences synaptic function and behavior in a maternal immune activation (MIA) model of SCZ.

Main Methods:

  • Identified single nucleotide polymorphisms (SNPs) in autophagy genes associated with SCZ.
  • Performed Gene Set Enrichment Analysis (GSEA) on public gene expression data.
  • Utilized a maternal immune activation (MIA) rat model, administering rapamycin or 3-Methyladenine (3-MA) during the weaning period.

Main Results:

  • Found 995 SNPs in 19 autophagy genes linked to SCZ and confirmed defective autophagy in SCZ patients via GSEA.
  • In the MIA rat model, autophagy was downregulated during weaning; early activation with rapamycin restored abnormal behaviors and electrophysiology.
  • Inhibition of autophagy with 3-MA led to aberrant behaviors, electrophysiological deficits, increased spine density, and impaired microglia-mediated synaptic pruning by disrupting complement signaling.

Conclusions:

  • Defective autophagy is significantly associated with SCZ.
  • Autophagy plays a critical role in regulating synaptic and behavioral deficits induced by MIA, particularly through microglia-mediated synaptic pruning and complement pathway regulation.