Characteristic phosphorylation of the extracellular signal-regulated kinase pathway after kainate-induced seizures in the rat hippocampus

Acta Neurochir Suppl. 2003;86:571-3. doi: 10.1007/978-3-7091-0651-8_116.


Extracellular signal-regulated kinase (ERK) pathways play a crucial role in cell growth and long-lasting neuronal plasticity. Several studies have shown that phosphorylated-ERK (p-ERK) significantly increases after kainic acid (KA) administration. However, little or no information is available about the spatial distribution of p-ERK after KA-induced seizures. We herein show that KA-induced seizures significantly increase p-ERK in both neurons and astrocytes in rat brain using Western blots and immunohistochemistry. A strong immunoreactivity for p-ERK was induced in the dentate hilar neurons and CA3 neurons 30 mins and 6 hrs after KA injection. In addition, immunoreactivity for p-ERK was seen in astrocytes 6 hrs after KA injection. 72 hrs after KA injection, all pyramidal neurons had died. These findings suggest that the ERK pathway participates in the KA-induced neurotoxicity in the rat hippocampus.

MeSH terms

  • Animals
  • Astrocytes / metabolism
  • Blotting, Western
  • Excitatory Amino Acid Agonists*
  • Hippocampus / cytology
  • Hippocampus / metabolism*
  • Immunohistochemistry / methods
  • Kainic Acid*
  • Male
  • Mitogen-Activated Protein Kinases / metabolism*
  • Neurons / metabolism
  • Phosphorylation
  • Rats
  • Rats, Sprague-Dawley
  • Seizures / chemically induced*
  • Seizures / metabolism*
  • Staining and Labeling


  • Excitatory Amino Acid Agonists
  • Mitogen-Activated Protein Kinases
  • Kainic Acid