Neurochemical Research

, Volume 13, Issue 1, pp 83–86

Decreased calmodulin kinase activity after status epilepticus

Authors

  • Jeff Bronstein
    • Department of NeuroscienceUCLA School of Medicine
  • Debora Farber
    • Department of OphthalmologyUCLA School of Medicine
  • Claude Wasterlain
    • Department of NeuroscienceUCLA School of Medicine
    • Department of NeurologyUCLA School of Medicine
Original Articles

DOI: 10.1007/BF00971859

Cite this article as:
Bronstein, J., Farber, D. & Wasterlain, C. Neurochem Res (1988) 13: 83. doi:10.1007/BF00971859

Abstract

Status epilepticus was induced in paralyzed, ventilated rats using bicuculline and was maintained for 50 to 120 minutes. Cerebral cortex, hippocampus, and cerebellum were assayed for calmodulin kinase II activity in vitro using [γ-32P]ATP and polyacrylamide gel electrophoresis. Seizures resulted in a 3.2 fold decrease in calmodulin kinase activity in crude synaptic membranes of cortex and in a 8.2 fold decrease in hippocampal membranes. Cytosolic calmodulin kinase activity was slightly increased in rats in status epilepticus but statistical significance was not reached. Status epilepticus did not affect calcium/calmodulin-dependent kinase activity in cerebellar membranes or cytosol. These data suggest that intense firing associated with continuous seizure activity decreases calmodulin kinase activity in cortical and hippocampal synaptic membranes, which may result in altered neuronal excitability.

Key Words

Calciumcalmodulin kinaseprotein phosphoylationepilepsystatus epilepticus

Copyright information

© Plenum Publishing Corporation 1987