regulation of action potential delays via voltage-gated potassium kv1.1 channels in dentate granule cells during hippocampal epilepsy

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ID: 251084
2013
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Abstract
Action potential (AP) responses of dentate gyrus granule (DG) cells have to be tightly regulated to maintain hippocampal function. However, which ion channels control the response delay of DG cells is not known. In some neuron types, spike latency is influenced by a dendrotoxin (DTX)-sensitive delay current (I<sub>D</sub>) mediated by unidentified combinations of voltage-gated K<sup>+</sup> (Kv) channels of the Kv1 family Kv1.1-6. In DG cells, the I<sub>D</sub> has not been characterized and its molecular basis is unknown. The response phenotype of mature DG cells is usually considered homogenous but intrinsic adaptations likely occur in particular in conditions of hyperexcitability, for example during temporal lobe epilepsy (TLE). In this study, we examined response delays of DG cells and underlying ion channel molecules by employing a new combination of gramicidin-perforated patch-clamp recordings in acute brain slices and single-cell reverse transcriptase quantitative polymerase chain reaction (SC RT-qPCR) experiments. An <i>in vivo</i> mouse model of TLE consisting of intrahippocampal kainate (KA) injection was used to examine epilepsy-related plasticity. Response delays of DG cells were DTX-sensitive and strongly increased in KA-injected hippocampi; Kv1.1 mRNA was elevated 10-fold, and the response delays correlated with Kv1.1 mRNA abundance on the single cell level. Other Kv1 subunits did not show overt changes in mRNA levels. Kv1.1 immunolabeling was enhanced in KA DG cells. The biophysical properties of I<sub>D</sub> and the delay heterogeneity between inner and outer DG cell layer were characterized. Using organotypic hippocampal slice cultures (OHCs), where KA incubation also induced I<sub>D</sub> upregulation, reversibility and neuroprotective potential for DG cells were tested. In summary, the AP timing of DG cells is effectively controlled via scaling of Kv1.1 subunit transcription. With this antiepileptic mechanism, DG cells delay their responses durin
Reference Key
ekirchheim2013frontiersregulation Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Florian eKirchheim;Florian eKirchheim;Stefanie eTinnes;Carola Anneliese Haas;Michael eStegen;Michael eStegen;Jakob eWolfart;Jakob eWolfart
Journal macromolecular bioscience
Year 2013
DOI
10.3389/fncel.2013.00248
URL
http://journal.frontiersin.org/Journal/10.3389/fncel.2013.00248/full
Keywords
hippocampus homeostasis kd neuropsychiatry biological psychiatry ammon’s horn sclerosisneurosciences

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