Hostname: page-component-586b7cd67f-2brh9 Total loading time: 0 Render date: 2024-11-22T10:50:34.419Z Has data issue: false hasContentIssue false
  • English
  • Français

Developmental and functional profile of the thalamic hyperpolarization-activated cation current, Ih, in absence epilepsy

Published online by Cambridge University Press:  05 February 2007

Hans-Christian Pape ,
Tatyana Kanyshkova ,
Tilman Broicher  and
Thomas Budde
Hans-Christian Pape
Affiliation:
Institut für Physiologie I, Germany
Tatyana Kanyshkova
Affiliation:
Institut für Physiologie I, Germany
Tilman Broicher
Affiliation:
Institut für Physiologie I, Germany
Thomas Budde
Affiliation:
Institut für Experimentelle Epilepsieforschung, Westfälische Wilhelms-Universität Münster, Germany
Get access Rights & Permissions [Opens in a new window]

Abstract

Recent findings in two rat models of absence epilepsy, the Wistar Albino Glaxo Rats from Rijswik (WAG/Rij) and the Genetic Absence Epilepsy Rats from Strasbourg (GAERS), support the idea that defects in the function of hyperpolarization-activated, cyclic nucleotide-gated cation channels (HCN1-4) and the resulting membrane current, Ih, in thalamocortical relay neurons are crucially involved in epilepsy. After a developmental evolution the expression of HCN1, which is relatively insensitive to cAMP, is elevated significantly in epileptic rats with no changes in expression of the other isoforms. This is accompanied by a hyperpolarizing shift in Ih activation and reduced sensitivity to cAMP. Thus, modification of thalamic Ih occurs at pre-epileptic stages and seems to be crucial to the development of spike-and-wave-discharges that characterize absence seizures.

Keywords

HCN channelscAMPpatch-clampin situ hybridizationchannelopathy
Type
Research Article
Information
Thalamus & Related Systems , Volume 3 , Issue 3 , September 2005 , pp. 175 - 180
Copyright
2007 Cambridge University Press

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)