Increased vulnerability to kainic acid-induced epileptic seizures in mice underexpressing the scaffold protein Islet-Brain 1/JIP-1

Eur J Neurosci. 2003 Jun;17(12):2602-10. doi: 10.1046/j.1460-9568.2003.02701.x.

Abstract

Islet-Brain 1, also known as JNK-interacting protein-1 (IB1/JIP-1) is a scaffold protein mainly involved in the regulation of the pro-apoptotic signalling cascade mediated by c-Jun-N-terminal kinase (JNK). IB1/JIP-1 organizes JNK and upstream kinases in a complex that facilitates JNK activation. However, overexpression of IB1/JIP-1 in neurons in vitro has been reported to result in inhibition of JNK activation and protection against cellular stress and apoptosis. The occurrence and the functional significance of stress-induced modulations of IB1/JIP-1 levels in vivo are not known. We investigated the regulation of IB1/JIP-1 in mouse hippocampus after systemic administration of kainic acid (KA), in wild-type mice as well as in mice hemizygous for the gene MAPK8IP1, encoding for IB1/JIP-1. We show here that IB1/JIP-1 is upregulated transiently in the hippocampus of normal mice, reaching a peak 8 h after seizure induction. Heterozygous mutant mice underexpressing IB1/JIP-1 showed a higher vulnerability to the epileptogenic properties of KA, whereas hippocampal IB1/JIP-1 levels remained unchanged after seizure induction. Subsequently, an increasing activation of JNK in the 8 h following seizure induction was observed in IB1/JIP-1 haploinsufficient mice, which also underwent more severe excitotoxic lesions in hippocampal CA3, as assessed histologically 3 days after KA administration. Taken together, these data indicate that IB1/JIP-1 in hippocampus participates in the regulation of the neuronal response to excitotoxic stress in a level-dependent fashion.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing*
  • Animals
  • Blotting, Western / methods
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism*
  • Cell Death
  • Cell Nucleus / pathology
  • Cytoplasm / pathology
  • Epilepsy / chemically induced
  • Epilepsy / metabolism*
  • Excitatory Amino Acid Agonists / administration & dosage*
  • Female
  • Gene Expression / drug effects
  • Hippocampus / metabolism*
  • Hippocampus / ultrastructure
  • Immunohistochemistry / methods
  • In Situ Nick-End Labeling / methods
  • Kainic Acid / adverse effects*
  • Kainic Acid / analogs & derivatives
  • Male
  • Mice
  • Mice, Inbred Strains
  • Mice, Mutant Strains
  • Microscopy, Electron / instrumentation
  • Microscopy, Electron / methods
  • Time Factors

Substances

  • Adaptor Proteins, Signal Transducing
  • Carrier Proteins
  • Excitatory Amino Acid Agonists
  • Mapk8ip protein, mouse
  • Kainic Acid