Reduced Reelin Expression in the Hippocampus after Traumatic Brain Injury. Academic Article uri icon

Overview

abstract

  • Traumatic brain injury (TBI) is a relatively common occurrence following accidents or violence, and often results in long-term cognitive or motor disability. Despite the high health cost associated with this type of injury, presently there are no effective treatments for many neurological symptoms resulting from TBI. This is due in part to our limited understanding of the mechanisms underlying brain dysfunction after injury. In this study, we used the mouse controlled cortical impact (CCI) model to investigate the effects of TBI, and focused on Reelin, an extracellular protein that critically regulates brain development and modulates synaptic activity in the adult brain. We found that Reelin expression decreases in forebrain regions after TBI, and that the number of Reelin-expressing cells decrease specifically in the hippocampus, an area of the brain that plays an important role in learning and memory. We also conducted in vitro experiments using mouse neuronal cultures and discovered that Reelin protects hippocampal neuronal cells from glutamate-induced neurotoxicity, a well-known secondary effect of TBI. Together our findings suggest that the loss of Reelin expression may contribute to neuronal death in the hippocampus after TBI, and raise the possibility that increasing Reelin levels or signaling activity may promote functional recovery.

publication date

  • June 29, 2020

Research

keywords

  • Brain Injuries, Traumatic
  • Cell Adhesion Molecules, Neuronal
  • Down-Regulation
  • Extracellular Matrix Proteins
  • Hippocampus
  • Nerve Tissue Proteins
  • Serine Endopeptidases

Identity

PubMed Central ID

  • PMC7407987

Scopus Document Identifier

  • 85087165544

Digital Object Identifier (DOI)

  • 10.1016/j.neuroscience.2011.05.050

PubMed ID

  • 32610618

Additional Document Info

volume

  • 10

issue

  • 7