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首页> 外文期刊>American Journal of Physiology >Response of catecholaminergic neurons in the mouse hindbrain to glucoprivic stimuli is astrocyte dependent
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Response of catecholaminergic neurons in the mouse hindbrain to glucoprivic stimuli is astrocyte dependent

机译：在小鼠后脑中的儿茶酚胺能神经元对葡萄糖刺激的反应是星形胶质细胞依赖性

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Hindbrain catecholaminergic (CA) neurons are required for critical autonomic, endocrine, and behavioral counterregulatory responses (CRRs) to hypoglycemia. Recent studies suggest that CRR initiation depends on hindbrain astrocyte glucose sensors (McDougal DH, Hermann GE, Rogers RC. Front Neurosci 7: 249, 2013; Rogers RC, Ritter S, Hermann GE. Am J Physiol Regul Integr Comp Physiol 310: R1102–R1108, 2016). To test the proposition that hindbrain CA responses to glucoprivation are astrocyte dependent, we utilized transgenic mice in which the calcium reporter construct (GCaMP5) was expressed selectively in tyrosine hydroxylase neurons (TH-GCaMP5). We conducted live cell calcium-imaging studies on tissue slices containing the nucleus of the solitary tract (NST) or the ventrolateral medulla, critical CRR initiation sites. Results show that TH-GCaMP5 neurons are robustly activated by a glucoprivic challenge and that this response is dependent on functional astrocytes. Pretreatment of hindbrain slices with fluorocitrate (an astrocytic metabolic suppressor) abolished TH-GCaMP5 neuronal responses to glucoprivation, but not to glutamate. Pharmacologic results suggest that the astrocytic connection with hindbrain CA neurons is purinergic via P2 receptors. Parallel imaging studies on hindbrain slices of NST from wild-type C57BL/6J mice, in which astrocytes and neurons were prelabeled with a calcium reporter dye and an astrocytic vital dye, show that both cell types are activated by glucoprivation but astrocytes responded significantly sooner than neurons. Pretreatment of these hindbrain slices with P2 antagonists abolished neuronal responses to glucoprivation without interruption of astrocyte responses; pretreatment with fluorocitrate eliminated both astrocytic and neuronal responses. These results support earlier work suggesting that the primary detection of glucoprivic signals by the hindbrain is mediated by astrocytes.
机译：临界自主主义，内分泌和行为反应性反应（CRRS）需要后脑摄入剂的神经元（CA）对低血糖症需要的。最近的研究表明，CRR启动取决于后脑星形细胞葡萄糖传感器（麦克风DH，Hermann GE，Rogers RC。前Neurosci 7：249,2013; Rogers RC，Ritter S，Hermann Ge。AM J Physiol Seng Integr Comp Physiol 310：R1102- R1108,2016）。为了测试后脑Ca反应对葡萄糖的命题是过度的，我们利用了在酪氨酸羟化酶神经元（Th-Gcamp5）中选择性地表达钙报告器构建体（Gcamp5）的转基因小鼠。我们对含有孤立菌（NST）或腹外侧髓质的核，关键CRR起始位点的核的组织切片进行了活细胞钙成像研究。结果表明，TH-GCAMP5神经元由葡萄糖挑战强烈激活，并且这种反应依赖于功能性星形胶质细胞。用氟柠檬酸盐（星形胶合质代谢抑制剂）预处理的预处理（星形胶合致代谢抑制剂）废除了对葡萄糖的TH-GCAMP5神经元反应，而不是谷氨酸。药理学结果表明，与后脑Ca神经元的星形胶合性联系是P2受体的纯化学能。来自野生型C57BL / 6J小鼠的正链切片的平行成像研究，其中星形胶质细胞和神经元用钙报告染料和星形胶质细胞至关重要的染料预订，表明两种细胞类型都是通过葡萄糖激活但星形胶质细胞比神经元。使用P2拮抗剂的预处理与P2拮抗剂废除了对葡萄糖的神经元反应而不会中断星形胶质细胞应答;用氟柠檬酸酯预处理消除了星形胶质细胞和神经元反应。这些结果支持前面的工作表明，通过星形胶质细胞介导的后脑介导葡萄糖信号的主要检测。

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