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http://purl.uniprot.org/citations/22504905http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22504905http://www.w3.org/2000/01/rdf-schema#comment"

Aim

To identify the mechanisms underlying the elevation of intracellular Ca(2+) level ([Ca(2+)](i)) induced by lowering extracellular glucose in rat hypothalamic arcuate nucleus NPY neurons.

Methods

Primary cultures of hypothalamic arcuate nucleus (ARC) neurons were prepared from Sprague-Dawley rats. NPY neurons were identified with immunocytochemical method. [Ca(2+)](i) was measured using fura-2 AM. Ca(2+) current was recorded using whole-cell patch clamp recording. AMPK and GSK3β levels were measured using Western blot assay.

Results

Lowering glucose level in the medium (from 10 to 1 mmol/L) induced a transient elevation of [Ca(2+)](i) in ARC neurons, but not in hippocampal and cortical neurons. The low-glucose induced elevation of [Ca(2+)](i) in ARC neurons depended on extracellular Ca(2+), and was blocked by P/Q-type Ca(2+)channel blocker ω-agatoxin TK (100 nmol/L), but not by L-type Ca(2+) channel blocker nifedipine (10 μmol/L) or N-type Ca(2+)channel blocker ω-conotoxin GVIA (300 nmol/L). Lowering glucose level increased the peak amplitude of high voltage-activated Ca(2+) current in ARC neurons. The low-glucose induced elevation of [Ca(2+)](i) in ARC neurons was blocked by the AMPK inhibitor compound C (20 μmol/L), and enhanced by the GSK3β inhibitor LiCl (10 mmol/L). Moreover, lowering glucose level induced the phosphorylation of AMPK and GSK3β, which was inhibited by compound C (20 μmol/L).

Conclusion

Lowering glucose level enhances the activity of P/Q type Ca(2+)channels and elevates [Ca(2+)](i) level in hypothalamic arcuate nucleus neurons via inhibition of GSK3β."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.org/dc/terms/identifier"doi:10.1038/aps.2012.17"xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/author"Jin Y."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/author"Ni L."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/author"Huang C."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/author"Zhou J."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/author"Wang F."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/author"Chen J.G."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/author"Zhang J.Q."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/author"Xie N."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/author"Hu Z.L."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/author"Long L.H."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/name"Acta Pharmacol Sin"xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/pages"594-605"xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/title"Lowering glucose level elevates [Ca2+]i in hypothalamic arcuate nucleus NPY neurons through P/Q-type Ca2+ channel activation and GSK3beta inhibition."xsd:string
http://purl.uniprot.org/citations/22504905http://purl.uniprot.org/core/volume"33"xsd:string
http://purl.uniprot.org/citations/22504905http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22504905
http://purl.uniprot.org/citations/22504905http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22504905
http://purl.uniprot.org/uniprot/#_P54282-mappedCitation-22504905http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22504905
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