| http://purl.uniprot.org/citations/15175395 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15175395 | http://www.w3.org/2000/01/rdf-schema#comment | "Alterations in thalamic T-type Ca2+ channels are thought to contribute to the pathogenesis of absence seizures. Here, we found that mice with a null mutation for the pore-forming alpha1A subunits of P/Q-type channels (alpha1A-/-mice) were prone to absence seizures characterized by typical spike-and-wave discharges (SWDs) and behavioral arrests. Isolated thalamocortical relay (TC) neurons from these mice showed increased T-type Ca2+ currents in vitro. To examine the role of increased T-currents in alpha1A-/-TC neurons, we cross-bred alpha1A-/-mice with mice harboring a null mutation for the gene encoding alpha1G, a major isotype of T-type Ca2+ channels in TC neurons. alpha1A-/-/alpha1G-/-mice showed a complete loss of T-type Ca2+ currents in TC neurons and displayed no SWDs. Interestingly, alpha1A-/-/alpha1G+/-mice had 75% of the T-type Ca2+ currents in TC neurons observed in alpha1A+/+/alpha1G+/+ mice and showed SWD activity that was quantitatively similar to that in alpha1A-/-/alpha1G+/+ mice. Similar results were obtained using double-mutant mice harboring the alpha1G mutation plus another mutation also used as a model for absence seizures, i.e., lethargic (beta4(lh/lh)), tottering (alpha1A(tg/tg)), or stargazer (gamma2(stg/stg)). The present results reveal that alpha1G T-type Ca2+ channels play a critical role in the genesis of spontaneous absence seizures resulting from hypofunctioning P/Q-type channels, but that the augmentation of thalamic T-type Ca2+ currents is not an essential step in the genesis of absence seizures."xsd:string |
| http://purl.uniprot.org/citations/15175395 | http://purl.org/dc/terms/identifier | "doi:10.1523/jneurosci.5546-03.2004"xsd:string |
| http://purl.uniprot.org/citations/15175395 | http://purl.uniprot.org/core/author | "Choi S."xsd:string |
| http://purl.uniprot.org/citations/15175395 | http://purl.uniprot.org/core/author | "Kim Y."xsd:string |
| http://purl.uniprot.org/citations/15175395 | http://purl.uniprot.org/core/author | "Kim D."xsd:string |
| http://purl.uniprot.org/citations/15175395 | http://purl.uniprot.org/core/author | "Sun M."xsd:string |
| http://purl.uniprot.org/citations/15175395 | http://purl.uniprot.org/core/author | "Shin H.S."xsd:string |
| http://purl.uniprot.org/citations/15175395 | http://purl.uniprot.org/core/author | "Song I."xsd:string |
| http://purl.uniprot.org/citations/15175395 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15175395 | http://purl.uniprot.org/core/name | "J Neurosci"xsd:string |
| http://purl.uniprot.org/citations/15175395 | http://purl.uniprot.org/core/pages | "5249-5257"xsd:string |
| http://purl.uniprot.org/citations/15175395 | http://purl.uniprot.org/core/title | "Role of the alpha1G T-type calcium channel in spontaneous absence seizures in mutant mice."xsd:string |
| http://purl.uniprot.org/citations/15175395 | http://purl.uniprot.org/core/volume | "24"xsd:string |
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