Abstract| Volume 46, P55, May 2015

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Antiepileptic action of c-Jun N-terminal kinase (JNK) inhibition

      We have been studying the role of hyperpolarization-activated (HCN) ion channels in epilepsy and the mechanisms underlying their chronic downregulation. We published findings (Jung et al., J. Neurosci., 2010) that downregulation of HCN channel gating in chronic epilepsy was associated in part with decreased activity of p38 mitogen-activated kinase (p38 MAPK). Although this phosphorylation pathway affects numerous cellular processes, we asked whether pharmacological reversal of the p38 MAPK activation deficit in vivo might produce an antiepileptic benefit in chronically epileptic animals.
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