| pubmed-article:19508695 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C0205102 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C0017725 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C0235169 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C1442161 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C1113688 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C1415500 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C1416596 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C1416601 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
| pubmed-article:19508695 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:19508695 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:19508695 | pubmed:dateCreated | 2009-7-7 | lld:pubmed |
| pubmed-article:19508695 | pubmed:abstractText | The firing of hypothalamic hypocretin/orexin neurons is vital for normal sleep-wake transitions, but its molecular determinants are not well understood. It was recently proposed that TASK (TWIK-related acid-sensitive potassium) channels [TASK1 (K(2P)3.1) and/or TASK3 (K(2P)9.1)] regulate neuronal firing and may contribute to the specialized responses of orexin neurons to glucose and pH. Here we tested these theories by performing patch-clamp recordings from orexin neurons directly identified by targeted green fluorescent protein labelling in brain slices from TASK1/3 double-knockout mice. The deletion of TASK1/3 channels significantly reduced the ability of orexin cells to generate high-frequency firing. Consistent with reduced excitability, individual action potentials from knockout cells had lower rates of rise, higher thresholds and more depolarized after-hyperpolarizations. However, orexin neurons from TASK1/3 knockout mice retained typical responses to glucose and pH, and the knockout animals showed normal food-anticipatory locomotor activity. Our results support a novel role for TASK genes in enhancing neuronal excitability and promoting high-frequency firing, but suggest that TASK1/3 subunits are not essential for orexin cell responses to glucose and pH. | lld:pubmed |
| pubmed-article:19508695 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19508695 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19508695 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19508695 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19508695 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:19508695 | pubmed:issn | 1460-9568 | lld:pubmed |
| pubmed-article:19508695 | pubmed:author | pubmed-author:GonzálezJ AJA | lld:pubmed |
| pubmed-article:19508695 | pubmed:author | pubmed-author:MenakerMichae... | lld:pubmed |
| pubmed-article:19508695 | pubmed:author | pubmed-author:FuggerLarsL | lld:pubmed |
| pubmed-article:19508695 | pubmed:author | pubmed-author:BaylissDougla... | lld:pubmed |
| pubmed-article:19508695 | pubmed:author | pubmed-author:BurdakovDenis... | lld:pubmed |
| pubmed-article:19508695 | pubmed:author | pubmed-author:DoyleSusan... | lld:pubmed |
| pubmed-article:19508695 | pubmed:author | pubmed-author:Miranda-Anaya... | lld:pubmed |
| pubmed-article:19508695 | pubmed:author | pubmed-author:JensenLise... | lld:pubmed |
| pubmed-article:19508695 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19508695 | pubmed:volume | 30 | lld:pubmed |
| pubmed-article:19508695 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19508695 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19508695 | pubmed:pagination | 57-64 | lld:pubmed |
| pubmed-article:19508695 | pubmed:dateRevised | 2011-6-6 | lld:pubmed |
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| pubmed-article:19508695 | pubmed:meshHeading | pubmed-meshheading:19508695... | lld:pubmed |
| pubmed-article:19508695 | pubmed:meshHeading | pubmed-meshheading:19508695... | lld:pubmed |
| pubmed-article:19508695 | pubmed:meshHeading | pubmed-meshheading:19508695... | lld:pubmed |
| pubmed-article:19508695 | pubmed:meshHeading | pubmed-meshheading:19508695... | lld:pubmed |
| pubmed-article:19508695 | pubmed:meshHeading | pubmed-meshheading:19508695... | lld:pubmed |
| pubmed-article:19508695 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19508695 | pubmed:articleTitle | Deletion of TASK1 and TASK3 channels disrupts intrinsic excitability but does not abolish glucose or pH responses of orexin/hypocretin neurons. | lld:pubmed |
| pubmed-article:19508695 | pubmed:affiliation | Department of Pharmacology, University of Cambridge, Cambridge CB2 1 PD, UK. | lld:pubmed |
| pubmed-article:19508695 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19508695 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:19508695 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:19508695 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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