The mGluR5-mediated Arc activation protects against experimental traumatic brain injury in rats.

ABSTRACT:

Introduction

Traumatic brain injury (TBI) is a complex pathophysiological process, and increasing attention has been paid to the important role of post-synaptic density (PSD) proteins, such as glutamate receptors. Our previous study showed that a PSD protein Arc/Arg3.1 (Arc) regulates endoplasmic reticulum (ER) stress and neuronal necroptosis in traumatic injury in vitro.

Aim

In this study, we investigated the expression, regulation and biological function of Arc in both in vivo and in vitro experimental TBI models.

Results

Traumatic neuronal injury (TNI) induced a temporal upregulation of Arc in cortical neurons, while TBI resulted in sustained increase in Arc expression up to 24 h in rats. The increased expression of Arc was mediated by the activity of metabotropic

SUBMITTER: Chen T 

PROVIDER: S-EPMC11303269 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature