TNF-alpha receptor 1 deficiency enhances kainic acid-induced hippocampal injury in mice

J Neurosci Res. 2008 May 15;86(7):1608-14. doi: 10.1002/jnr.21600.

Abstract

The exact role of TNF-alpha in excitotoxic neurodegeneration of the brain is unclear. To address this issue, the kainic acid (KA)-induced hippocampal injury model, a well-characterized model of human neurodegenerative diseases, was used in TNF-alpha receptor 1 (TNFR1)-knockout (TNFR1-/-) mice in the present study. After nasal application of a single dose of 40 mg of KA per kilogram body weight, TNFR1-/- mice showed significantly more severe seizures than the wild-type mice. In addition, obvious neurodegeneration, enhanced microglia activation, and astrogliosis in the hippocampus, as well as increased locomotor activity, were found in TNFR1-/- mice compared with the wild-type controls 8 days after KA delivery. Moreover, CC chemokine receptor 3 expression on activated microglia was increased 3 days after KA treatment in TNFR1-/- mice, as measured by flow cytometry. These data suggest that TNF-alpha may play a protective role through TNFR1 signaling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Behavior, Animal
  • Brain Injuries / chemically induced*
  • Brain Injuries / genetics
  • Brain Injuries / pathology
  • Brain Injuries / physiopathology
  • CD11b Antigen / metabolism
  • Case-Control Studies
  • Exploratory Behavior / drug effects
  • Exploratory Behavior / physiology
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / genetics
  • Glial Fibrillary Acidic Protein / genetics
  • Glial Fibrillary Acidic Protein / metabolism
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Hippocampus / pathology*
  • Kainic Acid*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Microglia / drug effects
  • Microglia / metabolism
  • Motor Activity / drug effects
  • Motor Activity / genetics
  • Neurodegenerative Diseases / chemically induced
  • Neurodegenerative Diseases / genetics
  • Neurodegenerative Diseases / physiopathology
  • Receptors, Tumor Necrosis Factor, Type I / deficiency*
  • Seizures / chemically induced

Substances

  • CD11b Antigen
  • Glial Fibrillary Acidic Protein
  • Receptors, Tumor Necrosis Factor, Type I
  • Kainic Acid