Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy
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 inte...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2008-10-01
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| Series: | Neurobiology of Disease |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0969996108001289 |
| _version_ | 1828967266639675392 |
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| author | Minyoung Shin Darrin Brager Thomas C. Jaramillo Daniel Johnston Dane M. Chetkovich |
| author_facet | Minyoung Shin Darrin Brager Thomas C. Jaramillo Daniel Johnston Dane M. Chetkovich |
| author_sort | Minyoung Shin |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-14T11:46:50Z |
| format | Article |
| id | doaj.art-17923c04ce5d40629a7c5c80559e0c8b |
| institution | Directory Open Access Journal |
| issn | 1095-953X |
| language | English |
| last_indexed | 2024-12-14T11:46:50Z |
| publishDate | 2008-10-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Neurobiology of Disease |
| spelling | doaj.art-17923c04ce5d40629a7c5c80559e0c8b2022-12-21T23:02:31ZengElsevierNeurobiology of Disease1095-953X2008-10-013212636Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsyMinyoung Shin0Darrin Brager1Thomas C. Jaramillo2Daniel Johnston3Dane M. Chetkovich4Davee Department of Neurology and Clinical Neurosciences, Feinberg School of Medicine, Northwest University Medical School, Chicago, IL 60611, USACenter for Learning and Memory, Section of Neurobiology, University of Texas at Austin, Austin, Texas 78712, USADavee Department of Neurology and Clinical Neurosciences, Feinberg School of Medicine, Northwest University Medical School, Chicago, IL 60611, USACenter for Learning and Memory, Section of Neurobiology, University of Texas at Austin, Austin, Texas 78712, USADavee Department of Neurology and Clinical Neurosciences, Feinberg School of Medicine, Northwest University Medical School, Chicago, IL 60611, USA; Department of Physiology, Feinberg School of Medicine, Northwestern University Medical School, Chicago, IL 60611, USA; Corresponding author. Davee Department of Neurology and Clinical Neuroscience, Northwestern University Medical School, 303 East Chicago Avenue, Ward 10-201, Chicago, IL 60611-3008, USA. Fax: +1 312 503 0872.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.http://www.sciencedirect.com/science/article/pii/S0969996108001289EpilepsySeizureHyperpolarization-activated cyclicNucleotide-gated channelKainic acid |
| spellingShingle | Minyoung Shin Darrin Brager Thomas C. Jaramillo Daniel Johnston Dane M. Chetkovich Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy Neurobiology of Disease Epilepsy Seizure Hyperpolarization-activated cyclic Nucleotide-gated channel Kainic acid |
| title | Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy |
| title_full | Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy |
| title_fullStr | Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy |
| title_full_unstemmed | Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy |
| title_short | Mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy |
| title_sort | mislocalization of h channel subunits underlies h channelopathy in temporal lobe epilepsy |
| topic | Epilepsy Seizure Hyperpolarization-activated cyclic Nucleotide-gated channel Kainic acid |
| url | http://www.sciencedirect.com/science/article/pii/S0969996108001289 |
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