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Neurobehavioral Assessments in a Mouse Model of Neonatal Hypoxic-ischemic Brain Injury
08:32

Neurobehavioral Assessments in a Mouse Model of Neonatal Hypoxic-ischemic Brain Injury

Published on: November 24, 2017

12.9K

GluR1 protects hypoxic ischemic brain damage via activating Akt signaling pathway in neonatal rats

J-Z Huang1, Y Ren, Y Jiang

  • 1Department of Neurology, Department of Endocrinology; the Third Affiliated Hospital of Soochow University, Changzhou, China. feihua_changzhou@126.com.

European Review for Medical and Pharmacological Sciences
|December 22, 2018
PubMed

Insights

Glutamic acid receptor 1 (GluR1) protects against neonatal hypoxic-ischemic brain damage (HIBD). Inhibiting GluR1 increased cell apoptosis, suggesting its protective role via Akt signaling and VEGF upregulation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Developmental Biology

Background:

  • Hypoxic-ischemic brain damage (HIBD) is a significant cause of neonatal mortality and long-term neurological deficits.
  • Glutamic acid receptor 1 (GluR1) plays a critical role in synaptic plasticity and neuronal function.
  • The specific role of GluR1 in HIBD remains to be fully elucidated.

Purpose of the Study:

  • To investigate the neuroprotective role of GluR1 in neonatal rat models of HIBD.
  • To explore the underlying molecular mechanisms involving the Akt signaling pathway and vascular endothelial growth factor (VEGF).

Main Methods:

  • Neonatal rats underwent common carotid artery ligation to induce HIBD.
  • Lentivirus-mediated shRNA was used to inhibit GluR1 expression in vivo.
  • Western blot analysis was performed to quantify protein levels of GluR1, p-Akt, and VEGF.
  • Cell apoptosis was assessed using TUNEL staining.

Main Results:

  • GluR1 expression significantly increased after HIBD, peaking at 24 hours.
  • Inhibition of GluR1 via shRNA transfection led to increased cell apoptosis.
  • Downregulation of GluR1 also reduced the expression of p-Akt and VEGF following HIBD.

Conclusions:

  • GluR1 demonstrates a significant protective effect against HIBD in neonatal rats.
  • This protective role is likely mediated by the activation of the Akt signaling pathway and the upregulation of VEGF.
Abstract

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