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Related Experiment Video

Updated: Dec 16, 2025

Biomarkers in an Animal Model for Revealing Neural, Hematologic, and Behavioral Correlates of PTSD
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RAGE Signaling pathway in hippocampus dentate gyrus involved in GLT-1 decrease induced by chronic unpredictable

Fang Yang1, Hong Wang1, Huali Chen1

  • 1Key Laboratory of Molecular and Biochemical Pharmacology, School of Pharmacy, Chongqing Medical University, Chongqing, China.

Brain Research Bulletin
|July 5, 2020
PubMed
Summary

Chronic unpredictable stress (CUS) induces depressive-like behaviors by reducing the receptor for advanced glycosylation end products (RAGE) and glutamate transporter-1 (GLT-1) in the hippocampus. This suggests a novel RAGE/CREB-NF-κB pathway involved in major depressive disorder pathophysiology.

Keywords:
Chronic unpredictable stressGLT-1Glutamate transporter-1Major depressive disorderRAGEReceptors for advanced glycosylation end products

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Psychiatry

Background:

  • Glutamatergic neurotransmission is implicated in major depressive disorder (MDD).
  • Glutamate transporters regulate glutamate homeostasis, and their downregulation is observed in MDD.
  • Mechanisms of stress-induced glutamate transporter modulation remain unclear.

Purpose of the Study:

  • To investigate the role of the Receptor for Advanced Glycation End Products (RAGE) in stress-induced depressive-like behaviors.
  • To elucidate the involvement of the RAGE/CREB-NF-κB signaling pathway in regulating glutamate transporter-1 (GLT-1) expression in the hippocampus.

Main Methods:

  • Chronic unpredictable stress (CUS) was applied to induce depressive-like behaviors in an animal model.
  • RAGE expression was knocked down in the hippocampus using RAGE shRNA lentivirus particles.
  • Protein and mRNA levels of RAGE, GLT-1, GLAST, CREB, and NF-κB (p65) were analyzed using Western blot and RT-qPCR.

Main Results:

  • CUS induced depressive-like behaviors and reduced RAGE, GLT-1, p-CREB, and p-p65 levels in the hippocampus.
  • RAGE knockdown in the hippocampus replicated depressive-like behaviors and decreased GLT-1 and p-CREB/p65 levels.
  • Neither CUS nor RAGE knockdown affected GLAST expression.

Conclusions:

  • The RAGE/CREB-NF-κB signaling pathway in the hippocampus modulates GLT-1 expression.
  • This pathway is implicated in the pathophysiology of CUS-induced depressive-like behaviors.
  • RAGE plays a critical role in regulating GLT-1 expression and stress responses relevant to MDD.