Journal article

Decreases in HCN mRNA expression in the hippocampus after kindling and status epilepticus in adult rats

Kim L Powell, Caroline Ng, Terence J O'Brien, Sheng Hong Xu, David A Williams, Simon J Foote, Christopher A Reid

EPILEPSIA | WILEY | Published : 2008

Abstract

PURPOSE: Studies in animal models and patients have implicated changes in hyperpolarization-activated cyclic nucleotide-gated cation channel (HCN) expression in the pathogenesis of temporal lobe epilepsy (TLE). However, the nature of HCN changes during the epileptogenic process and their commonality across different TLE models is unknown. Here HCN1 and HCN2 mRNA expression was quantitatively measured at different time points during epileptogenesis in two distinct animal models of TLE; the kainic acid (KA)-induced status epilepticus (SE) and amygdala kindling models. METHODS: Hippocampal subregions (CA1, CA3, and dentate gyrus [DG]) and entorhinal cortex were dissected at different time-point..

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Grants

Awarded by Australian National Health Medical Research Council (NHMRC)


Funding Acknowledgements

This study was in part supported by project grants from the Australian National Health and Medical Research Council (NH&MRC) to S. J Foote and T. J. O'Brien (Project Grant #406640) and C. A. Reid (Project Grant #454655) and a grant from the Royal Melbourne Hospital Neuroscience Foundation. C. A. Reid would like to acknowledge support from the Molly Me Donnell Foundation awarded by the Epilepsy Society of Australia.