Abstract
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. I(h), 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.
Publication types
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Comparative Study
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Channelopathies / metabolism*
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Channelopathies / pathology*
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Channelopathies / physiopathology
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Cyclic Nucleotide-Gated Cation Channels / metabolism*
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Cyclic Nucleotide-Gated Cation Channels / physiology
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Epilepsy, Temporal Lobe / metabolism*
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Epilepsy, Temporal Lobe / pathology*
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Epilepsy, Temporal Lobe / physiopathology
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Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
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Male
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Membrane Proteins / metabolism
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Membrane Proteins / physiology
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Mice
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Nerve Tissue Proteins / metabolism
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Nerve Tissue Proteins / physiology
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Potassium Channels / metabolism*
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Potassium Channels / physiology
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Protein Subunits / metabolism*
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Protein Subunits / physiology
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Protein Transport / genetics
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Rats
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Rats, Sprague-Dawley
Substances
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Cyclic Nucleotide-Gated Cation Channels
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Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
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Membrane Proteins
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Nerve Tissue Proteins
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Pex5l protein, rat
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Potassium Channels
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Protein Subunits