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Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy
We show here that the voltage-gated K(+) channel Kv12.2 is a potent regulator of excitability in hippocampal pyramidal neurons. Genetic deletion and pharmacologic block of Kv12.2 significantly reduced firing threshold in these neurons. Kv12.2(−/−) mice displayed signs of persistent neuronal hyperexc...
| Autores principales: | , , , , , , , , , , , , , |
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| Formato: | Texto |
| Lenguaje: | English |
| Publicado: |
2010
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| Materias: | |
| Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2928878/ https://www.ncbi.nlm.nih.gov/pubmed/20676103 http://dx.doi.org/10.1038/nn.2610 |
| _version_ | 1782185896865431552 |
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| author | Zhang, Xiaofei Bertaso, Federica Yoo, Jong W. Baumgärtel, Karsten Clancy, Sinead M. Lee, Van Cienfuegos, Cynthia Wilmot, Carly Avis, Jacqueline Hunyh, Truc Daguia, Catherine Schmedt, Christian Noebels, Jeffrey Jegla, Timothy |
| author_facet | Zhang, Xiaofei Bertaso, Federica Yoo, Jong W. Baumgärtel, Karsten Clancy, Sinead M. Lee, Van Cienfuegos, Cynthia Wilmot, Carly Avis, Jacqueline Hunyh, Truc Daguia, Catherine Schmedt, Christian Noebels, Jeffrey Jegla, Timothy |
| author_sort | Zhang, Xiaofei |
| collection | PubMed |
| description | We show here that the voltage-gated K(+) channel Kv12.2 is a potent regulator of excitability in hippocampal pyramidal neurons. Genetic deletion and pharmacologic block of Kv12.2 significantly reduced firing threshold in these neurons. Kv12.2(−/−) mice displayed signs of persistent neuronal hyperexcitability including frequent interictal spiking, spontaneous seizures and increased sensitivity to the chemoconvulsant pentylenetetrazol. |
| format | Text |
| id | pubmed-2928878 |
| institution | National Center for Biotechnology Information |
| language | English |
| publishDate | 2010 |
| record_format | MEDLINE/PubMed |
| spelling | pubmed-29288782011-03-01 Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy Zhang, Xiaofei Bertaso, Federica Yoo, Jong W. Baumgärtel, Karsten Clancy, Sinead M. Lee, Van Cienfuegos, Cynthia Wilmot, Carly Avis, Jacqueline Hunyh, Truc Daguia, Catherine Schmedt, Christian Noebels, Jeffrey Jegla, Timothy Nat Neurosci Article We show here that the voltage-gated K(+) channel Kv12.2 is a potent regulator of excitability in hippocampal pyramidal neurons. Genetic deletion and pharmacologic block of Kv12.2 significantly reduced firing threshold in these neurons. Kv12.2(−/−) mice displayed signs of persistent neuronal hyperexcitability including frequent interictal spiking, spontaneous seizures and increased sensitivity to the chemoconvulsant pentylenetetrazol. 2010-08-01 2010-09 /pmc/articles/PMC2928878/ /pubmed/20676103 http://dx.doi.org/10.1038/nn.2610 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms |
| spellingShingle | Article Zhang, Xiaofei Bertaso, Federica Yoo, Jong W. Baumgärtel, Karsten Clancy, Sinead M. Lee, Van Cienfuegos, Cynthia Wilmot, Carly Avis, Jacqueline Hunyh, Truc Daguia, Catherine Schmedt, Christian Noebels, Jeffrey Jegla, Timothy Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy |
| title | Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy |
| title_full | Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy |
| title_fullStr | Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy |
| title_full_unstemmed | Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy |
| title_short | Deletion of the potassium channel Kv12.2 causes hippocampal hyperexcitability and epilepsy |
| title_sort | deletion of the potassium channel kv12.2 causes hippocampal hyperexcitability and epilepsy |
| topic | Article |
| url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2928878/ https://www.ncbi.nlm.nih.gov/pubmed/20676103 http://dx.doi.org/10.1038/nn.2610 |
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