Lowering glucose level elevates Ca2+i in hypothalamic arcuate nucleus NPY neurons through P/Q-type Ca channel activation and GSK3β inhibition

Yu CHEN; Jian-guo CHEN; Li-hong LONG; Jun ZHOU; Na XIE; Chao HUANG; Jun-qi ZHANG; Zhuang-li HU; Lan NI; You JIN; Fang WANG

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Lowering glucose level elevates Ca2+i in hypothalamic arcuate nucleus NPY neurons through P/Q-type Ca channel activation and GSK3β inhibition

机译：葡萄糖水平降低通过P / Q型Ca通道激活和GSK3β抑制作用升高下丘脑弓状核NPY神经元中的Ca2 + i

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To identify the mechanisms underlying the elevation of intracellular Ca2+ level ([Ca2+]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.[Ca2+]i was measured using fura-2 AM.Ca2+ 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 [Ca2+]i in ARC neurons,but not in hippocampal and cortical neurons.The low-glucose induced elevation of [Ca2+]i in ARC neurons depended on extracellular Ca2+,and was blocked by P/Q-type Ca2+channel blocker ω-agatoxin TK (100 nmol/L),but not by L-type Ca2+ channel blocker nifedipine (10μmol/L) or N-type Ca2+ channel blocker ω-conotoxin GVIA (300 nmol/L).Lowering glucose level increased the peak amplitude of high voltage-activated Ca2+ current in ARC neurons.The low-glucose induced elevation of [Ca2+]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 Ca2+ channels and elevates [Ca2+]i level in hypothalamic arcuate nucleus neurons via inhibition of GSK3β.

机译：为了确定降低大鼠下丘脑弓状核NPY神经元细胞外葡萄糖诱导细胞内Ca2 +水平（[Ca2 +] i）升高的潜在机制。方法：从Sprague-Dawley大鼠中制备下丘脑弓状核（ARC）神经元原代培养物。 NPY神经元采用免疫细胞化学法鉴定，用fura-2 AM测定[Ca2 +] i，用全细胞膜片钳记录法记录Ca2 +电流，用Western blot法测定AMPK和GSK3β的水平。介质（从10到1 mmol / L）诱导ARC神经元中的[Ca2 +] i瞬时升高，但不引起海马和皮层神经元中的瞬时升高。低葡萄糖诱导ARC神经元中[Ca2 +] i的升高取决于细胞外Ca2 +，并被P / Q型Ca2 +通道阻滞剂ω-毒素TK（100 nmol / L）阻滞，但未被L型Ca2 +通道阻滞剂硝苯地平（10μmol/ L）或N型Ca2 +通道阻滞剂ω-芋螺毒素GVIA阻滞（300 nmol / L）。降低的葡萄糖水平增加低葡萄糖诱导的ARC神经元中Ca2 +电流的峰值。低糖诱导的ARC神经元中[Ca2 +] i的升高被AMPK抑制剂化合物C（20μmol/ L）阻断，并被GSK3β抑制剂LiCl增强（10 mmol / L）。此外，降低葡萄糖水平可诱导AMPK和GSK3β磷酸化，这被化合物C（20μmol/ L）抑制。结论：降低葡萄糖水平可增强P / Q型Ca2 +通道的活性并升高通过抑制GSK3β，下丘脑弓状核神经元中的[Ca2 +] i水平。

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《中国药理学报：英文版》 |2012年第5期|594-605|共12页
作者
Yu CHEN; Jian-guo CHEN; Li-hong LONG; Jun ZHOU; Na XIE; Chao HUANG; Jun-qi ZHANG; Zhuang-li HU; Lan NI; You JIN; Fang WANG;
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作者单位

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

Key Laboratory of Neurological Diseases, Huazhong University of Science and Technology, Ministry of Education of China, Wuhan 430030,China;

Institutes of Biomedcine and Drug Discovery, Huazhong University of Science and Technology, Wuhan 430030, China;

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

Key Laboratory of Neurological Diseases, Huazhong University of Science and Technology, Ministry of Education of China, Wuhan 430030,China;

Institutes of Biomedcine and Drug Discovery, Huazhong University of Science and Technology, Wuhan 430030, China;

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

Key Laboratory of Neurological Diseases, Huazhong University of Science and Technology, Ministry of Education of China, Wuhan 430030,China;

Institutes of Biomedcine and Drug Discovery, Huazhong University of Science and Technology, Wuhan 430030, China;

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

Key Laboratory of Neurological Diseases, Huazhong University of Science and Technology, Ministry of Education of China, Wuhan 430030,China;

Institutes of Biomedcine and Drug Discovery, Huazhong University of Science and Technology, Wuhan 430030, China;

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China;

Key Laboratory of Neurological Diseases, Huazhong University of Science and Technology, Ministry of Education of China, Wuhan 430030,China;

Institutes of Biomedcine and Drug Discovery, Huazhong University of Science and Technology, Wuhan 430030, China;

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Lowering glucose level elevates Ca2+i in hypothalamic arcuate nucleus NPY neurons through P/Q-type Ca channel activation and GSK3β inhibition

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