Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy

Minyoung Shin, Darrin Brager, Thomas C. Jaramillo, Daniel Johnston, Dane M. Chetkovich*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

74 Scopus citations


Many animal models of temporal lobe epilepsy (TLE) begin with status epilepticus (SE) followed by a latency period. Increased hippocampal pyramidal neuron excitability may contribute to seizures in TLE. Ih, mediated by h channels, regulates intrinsic membrane excitability by modulating synaptic integration and dampening dendritic calcium signaling. In a rat model of TLE, we found bidirectional changes in h channel function in CA1 pyramidal neurons. 1-2 d after SE, before onset of spontaneous seizures, physiological parameters dependent upon h channels were augmented and h channel subunit surface expression was increased. 28-30 d following SE, after onset of spontaneous seizures, h channel function in dendrites was reduced, coupled with diminished h channel subunit surface expression and relocalization of subunits from distal dendrites to soma. These results implicate h channel localization as a molecular mechanism influencing CA1 excitability in TLE.

Original languageEnglish (US)
Pages (from-to)26-36
Number of pages11
JournalNeurobiology of Disease
Issue number1
StatePublished - Oct 2008


  • Epilepsy
  • Hyperpolarization-activated cyclic
  • Kainic acid
  • Nucleotide-gated channel
  • Seizure

ASJC Scopus subject areas

  • Neurology

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