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Author Notes:

Correspondenceshould be addressed to Dr. Geidy E. Serrano, Banner Sun Health Research Institute, 10515 West Santa Fe Drive, Building B, 3rd Floor, Sun City, AZ 85351. E-mail: geidy.serrano@bannerhealth.com.

Author contributions: G.E.S., A.R., and R.D. designed research; G.E.S., N.L., A.R., S.C., R.S., C.D.M., and D.W. performed research; D.W. and G.A.F. contributed unpublished reagents/analytic tools; G.E.S., A.R., G.A.F., and R.D. analyzed data; G.E.S., A.R., and R.D. wrote the paper.

Subjects:

Research Funding:

This work was supported by the CounterACT Program, National Institutes of Health Office of the Director, and NINDS Grant U01NS058158 (R.D.), and by NIH Grants F32-NS064695 (G.E.S.), T32-DA015040 (A.R.), and P01 HL062250 (G.F.).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Neurosciences
  • Neurosciences & Neurology
  • TEMPORAL-LOBE EPILEPSY
  • DENTATE GRANULE CELLS
  • CXC CHEMOKINE LIGAND-10
  • CENTRAL-NERVOUS-SYSTEM
  • ACID-INDUCED SEIZURE
  • NF-KAPPA-B
  • RAT-BRAIN
  • GENE-EXPRESSION
  • LEUKOCYTE INFILTRATION
  • SYNAPTIC-TRANSMISSION

Ablation of Cyclooxygenase-2 in Forebrain Neurons is Neuroprotective and Dampens Brain Inflammation after Status Epilepticus

Tools:

Journal Title:

Journal of Neuroscience Nursing

Volume:

Volume 31, Number 42

Publisher:

, Pages 14850-14860

Type of Work:

Article | Final Publisher PDF

Abstract:

Cyclooxygenase-2 (COX-2), a source of inflammatory mediators and a multifunctional neuronal modulator, is rapidly induced in select populations of cortical neurons after status epilepticus. The consequences of rapid activity-triggered induction of COX-2 in neurons have been the subject of much study and speculation. To address this issue directly, we created a mouse in which COX-2 is conditionally ablated in selected forebrain neurons. Results following pilocarpine-induced status epilepticus indicate that neuronal COX-2 promotes early neuroprotection and then delayed neurodegeneration of CA1 pyramidal neurons, promotes neurodegeneration of nearby somatostatin interneurons in the CA1 stratum oriens and dentate hilus (which themselves do not express COX-2), intensifies a broad inflammatory reaction involving numerous cytokines and other inflammatory mediators in the hippocampus, and is essential for development of a leaky blood- brain barrier after seizures. These findings point to a profound role of seizure-induced neuronal COX-2 expression in neuropathologies that accompany epileptogenesis.

Copyright information:

© 2011 the authors.

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