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Lipidomics and Transcriptomics in Neurological Diseases
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Dysfunction of EAAT3 Aggravates LPS-Induced Post-Operative Cognitive Dysfunction.

Xiao-Yan Wang1,2, Wen-Gang Liu1,3, Ai-Sheng Hou3

  • 1Chinese PLA Medical School, Beijing 100853, China.

Membranes
|March 24, 2022
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Summary
This summary is machine-generated.

Inhibited excitatory amino acid transporter 3 (EAAT3) function worsens post-operative cognitive dysfunction (POCD). Riluzole treatment improved memory and EAAT3 function in elderly mice, suggesting EAAT3 as a promising POCD therapeutic target.

Keywords:
agingexcitatory amino acid transporter 3 (EAAT3)lipopolysaccharide (LPS)post-operative cognitive dysfunction (POCD)riluzole

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Inhibited excitatory amino acid transporter 3 (EAAT3) function is linked to neurodegenerative diseases and impaired learning/memory.
  • Post-operative cognitive dysfunction (POCD) is a significant concern, particularly in elderly patients.
  • Understanding the role of EAAT3 in POCD is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of EAAT3 in the development of POCD.
  • To explore the potential of riluzole in ameliorating POCD by targeting EAAT3 function.

Main Methods:

  • Established a mouse model of POCD using lipopolysaccharide (LPS) injection.
  • Utilized recombinant adeno-associated virus (rAAV)-mediated shRNA to knockdown EAAT3 expression in the hippocampus.
  • Administered riluzole to elderly male mice prior to LPS challenge.
  • Assessed cognitive function using the Morris water maze and performed pathological and biochemical analyses.

Main Results:

  • Hippocampal EAAT3 knockdown aggravated LPS-induced learning and memory deficits.
  • LPS inhibited EAAT3 membrane protein expression and GluA1 phosphorylation in adult mice.
  • Riluzole pretreatment increased hippocampal EAAT3 membrane protein expression and ameliorated cognitive impairment in elderly mice.

Conclusions:

  • EAAT3 dysfunction is a significant risk factor for POCD susceptibility.
  • Activating EAAT3 function with riluzole shows promise in treating POCD.
  • EAAT3 represents a potential therapeutic target for POCD intervention.