h experimentally induced seizures in rats and in patients with temporal lobe epilepsy. In instances of experimentally-produced prolonged seizures that damaged the hippocampus in rats, Bim expression increased. Blocking upstream activators of Bim or using Bim antisense to block Bim expression reduced neuronal damage. Of interest, in the hippocampus of epileptic patients, Bim appeared to be selectively down-regulated. These results suggest a means by which the brain may protect itself from additional neural damage following epileptic seizures. Targeting this molecular pathway may be worthwhile for ameliorating seizure-induced brain injuries.
An accompanying commentary by Jerome Niquet and Claude Wasterlain, of Epilepsy Research Laboratory, place this work in context with the complexity of cell-death pathways and highlight specific areas of future analysis that are still required to understand the molecular mechanisms at play in neuronal damage.
TITLE: Bim regulation may determine hippocampal vulnerability after injurious seizures and in temporal lobe epilepsy
David C. Henshall
Robert S. Dow Neurobiology Laboratories, Portland, Oregan, USA.
View the PDF of this article at: https://www.the-jci.org/press/19971.pdf
ACCOMPANYING COMMENTARY: Bim, Bad, and Bax: a deadly combination
in epileptic seizures
Epilepsy Research Laboratory, West Los Angeles, California, USA.
Phone: 310-478-3711 ext. 41974
View the PDF of this commentary at: https://www.the-jci.org/press/21478.pdf
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