Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1999-4-27
pubmed:abstractText
1. Patch-clamp recordings were made from rat ventromedial hypothalamic neurones in slices of brain tissue in vitro. In cell-attached recordings, removal of extracellular glucose or metabolic inhibition with sodium azide reduced the firing rate of a subpopulation of cells through the activation of a 65 pS channel that was blocked by the sulphonylureas tolbutamide and glibenclamide. 2. In whole-cell patch-clamp recordings, in the absence of ATP in the electrode solution, glucose-receptive neurones gradually hyperpolarized due to the induction of an outward current at -60 mV. This outward current and the resultant hyperpolarization were blocked by the sulphonylureas tolbutamide and glibenclamide. 3. In recordings where the electrode solution contained 4 mM ATP, this outward current was not observed. Under these conditions, 500 microM diazoxide was found to induce an outward current that was blocked by tolbutamide. 4. In cell-attached recordings diazoxide and the active fragment of leptin (leptin 22-56) reduced the firing rate of glucose-receptive neurones by the activation of a channel with similar properties to that induced by removal of extracellular glucose. 5. Reverse transcription followed by the polymerase chain reaction using cytoplasm from single glucose-receptive neurones demonstrated the expression of the ATP-sensitive potassium (KATP) channel subunits Kir6.1 and SUR1 but not Kir6.2 or SUR2. 6. It is concluded that glucose-receptive neurones within the rat ventromedial hypothalamus exhibit a KATP channel current with pharmacological and molecular properties similar to those reported in other tissues.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-1348109, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-14237464, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-1467829, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-1680516, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-2119205, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-2127550, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-2412077, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-2417160, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-2676059, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-2988416, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-3612561, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-6322917, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-7502040, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-7509437, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-7890693, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-8004407, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-8549751, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-9023770, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-9067450, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-9130167, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-9394003, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-9462882, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-9490811, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-9644047, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-9705995, http://linkedlifedata.com/resource/pubmed/commentcorrection/10050011-9742245
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-3751
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
515 ( Pt 2)
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
439-52
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Glucose-receptive neurones in the rat ventromedial hypothalamus express KATP channels composed of Kir6.1 and SUR1 subunits.
pubmed:affiliation
Parke Davis Neuroscience Research Centre, Cambridge University Forvie Site, Cambridge CB2 2QB, UK. kevin.lee@wl.com
pubmed:publicationType
Journal Article, In Vitro