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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Cholecystokinin activates orexin/hypocretin neurons through the cholecystokinin A receptor.
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Cholecystokinin activates orexin/hypocretin neurons through the cholecystokinin A receptor.

机译：胆囊收缩素通过胆囊收缩素A受体激活orexin / hypocretin神经元。

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摘要

Orexin A and B are neuropeptides implicated in the regulation of sleep/wakefulness and energy homeostasis. The regulatory mechanism of the activity of orexin neurons is not precisely understood. Using transgenic mice in which orexin neurons specifically express yellow cameleon 2.1, we screened for factors that affect the activity of orexin neurons (a total of 21 peptides and six other factors were examined) and found that a sulfated octapeptide form of cholecystokinin (CCK-8S), neurotensin, oxytocin, and vasopressin activate orexin neurons. The mechanisms that underlie CCK-8S-induced activation of orexin neurons were studied by both calcium imaging and slice patch-clamp recording. CCK-8S induced inward current in the orexin neurons. The CCKA receptor antagonist lorglumide inhibited CCK-8S-induced activation of orexin neurons, whereas the CCKB receptor agonists CCK-4 (a tetrapeptide form of cholecystokinin) and nonsulfated CCK-8 had little effect. The CCK-8S-induced increase in intracellular calcium concentration was eliminated by removing extracellular calcium but not by an addition of thapsigargin. Nifedipine, omega-conotoxin, omega-agatoxin, 4-ethylphenylamino-1,2-dimethyl-6-methylaminopyrimidinium chloride, and SNX-482 had little effect, but La3+, Gd3+, and 2-aminoethoxydiphenylborate inhibited CCK-8S-induced calcium influx. Additionally, the CCK-8S-induced inward current was dramatically enhanced in the calcium-free solution and was inhibited by the cation channel blocker SKF96365, suggesting an involvement of extracellular calcium-sensitive cation channels. CCK-8S did not induce an increase in intracellular calcium concentration when membrane potential was clamped at -60 mV, suggesting that the calcium increase is induced by depolarization. The evidence presented here expands our understanding of the regulation of orexin neurons and the physiological role of CCK in the CNS.
机译：食欲素A和B是神经肽，参与调节睡眠/清醒和能量稳态。食欲蛋白神经元活性的调节机制尚不清楚。使用其中orexin神经元特异表达黄色cameleon 2.1的转基因小鼠，我们筛选了影响orexin神经元活性的因子（共检查了21种肽和其他6种因子），发现硫酸八肽形式的胆囊收缩素（CCK-8S ），神经降压素，催产素和加压素激活食欲素神经元。通过钙成像和切片膜片钳记录研究了CCK-8S诱导的orexin神经元激活的基础机制。 CCK-8S在食欲素神经元中诱导内向电流。 CCKA受体拮抗剂lorglumide抑制CCK-8S诱导的食欲素神经元活化，而CCKB受体激动剂CCK-4（胆囊收缩素的四肽形式）和未硫酸化的CCK-8几乎没有作用。通过去除细胞外钙消除了CCK-8S诱导的细胞内钙浓度增加，但没有通过添加毒胡萝卜素来消除。硝苯地平，ω-芋螺毒素，ω-藻毒素，4-乙基苯基氨基-1,2-二甲基-6-甲基氨基嘧啶鎓氯化物和SNX-482作用不大，但La3 +，Gd3 +和2-氨基乙氧基二苯硼酸盐抑制了CCK-8S诱导的钙内流。此外，CCK-8S诱导的内向电流在无钙溶液中显着增强，并受到阳离子通道阻滞剂SKF96365的抑制，表明涉及细胞外钙敏感阳离子通道。当膜电位固定在-60 mV时，CCK-8S不会引起细胞内钙浓度的增加，这表明钙的增加是由去极化引起的。本文提供的证据扩大了我们对食欲素神经元调节和CCK在中枢神经系统中的生理作用的理解。

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