MK-801 inhibits the cortical increase in IGF-1, IGFBP-2 and IGFBP-4 expression following trauma

Neuroreport. 1997 Jan 20;8(2):455-60. doi: 10.1097/00001756-199701200-00016.

Abstract

Cerebral contusions increase cortical expression of insulin-like growth factor 1 (IGF-1), IGF binding protein-2 (IGFBP-2) and IGFBP-4, mRNA levels increase at the contusion site (IGF-1, IGFBP-2 and -4) and along the ipsilateral cortex (IGFBP-2 and -4). Here we explore whether this upregulation is glutamate dependent. Rats were treated with the non-competitive N-methyl-D-aspartate (NMDA) antagonist MK-801 or the non-NMDA antagonist CNQX before and after trauma, and analysed using quantitative in situ hybridization. The induction of IGF-1 expression was completely blocked by MK-801 or CNQX. IGFBP-2 mRNA levels remained high at the contusion site in the presence of either drug, but the increase was blocked in the cortex temporal to the impact by MK-801. The increase in IGFBP-4 mRNA was blocked by MK-801 but not by CNQX.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Injuries / metabolism*
  • Dizocilpine Maleate / pharmacology*
  • In Situ Hybridization
  • Insulin-Like Growth Factor Binding Protein 2 / drug effects*
  • Insulin-Like Growth Factor Binding Protein 2 / metabolism
  • Insulin-Like Growth Factor Binding Protein 4 / drug effects*
  • Insulin-Like Growth Factor Binding Protein 4 / metabolism
  • Insulin-Like Growth Factor I / drug effects*
  • Insulin-Like Growth Factor I / metabolism
  • Male
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Insulin-Like Growth Factor Binding Protein 2
  • Insulin-Like Growth Factor Binding Protein 4
  • Insulin-Like Growth Factor I
  • Dizocilpine Maleate