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Ablation of p27 enhance kainate-induced seizure and hippocampal degeneration

Chihiro Ueyama1, Hiroki Akashiba, Keiko Nakayama

  • 1Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan.

Neuroreport
|December 20, 2007
PubMed

Insights

Ablation of p27, a cell cycle inhibitor, enhances seizure and hippocampal cell death in mice following kainic acid treatment. This suggests p27 plays a protective role against excitotoxicity in the brain.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • p27 is a cyclin-dependent kinase inhibitor that regulates the cell cycle at the G1-S phase.
  • Previous studies showed that reducing p27 expression induces cell death in cultured neurons.
  • The in vivo role of p27 in neuronal response to excitotoxicity remains unclear.

Purpose of the Study:

  • To investigate the role of p27 in kainate-induced excitotoxicity in vivo.
  • To determine the effect of p27 deficiency on seizure activity and hippocampal cell death.

Main Methods:

  • Utilized p27 knockout mice (heterozygous and homozygous) and wild-type littermates.
  • Administered kainic acid to induce seizures and excitotoxicity.
  • Assessed hippocampal cell viability, seizure severity, and p27/retinoblastoma protein status.

Main Results:

  • Kainic acid induced p27 downregulation and retinoblastoma protein phosphorylation in wild-type hippocampus.
  • p27 knockout mice showed no difference in hippocampal cell viability without kainate treatment.
  • p27 homozygous mice exhibited exacerbated seizure activity and hippocampal degeneration post-kainic acid treatment.

Conclusions:

  • p27 deficiency enhances kainate-induced seizure and hippocampal cell death in vivo.
  • Ablation of p27 increases susceptibility to excitotoxic injury.
  • p27 may play a neuroprotective role in the context of excitotoxicity.

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