Norepinephrine controls both torpor initiation and emergence via distinct mechanisms in the mouse.
Norepinephrine controls both torpor initiation and emergence via distinct mechanisms in the mouse.
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DOI：
10.1371/journal.pone.0004038
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发表时间：
2008
期刊：
影响因子：
3.7
通讯作者：
Weinshenker D
中科院分区：
文献类型：
--
作者：
Swoap SJ;Weinshenker D
一些哺乳动物，包括实验室小鼠，在食物匮乏时会进入麻痹状态，而瘦素可以减轻这些麻痹发作。我们先前表明，多巴胺β-羟化酶敲除（Dbh −/−）小鼠，缺乏去甲肾上腺素（NE），禁食时不会减少循环瘦素，也不会进入麻痹状态。为了测试在禁食期间小鼠中麻痹的发作是否需要NE介导的循环瘦素的减少，产生瘦素（ob/ob）和DBH（DBL MUT）两者缺陷的双突变小鼠。禁食后，对照和ob/ob小鼠进入昏睡，如通过遥测核心Tb采集所评估的。虽然禁食不能诱导Dbh −/−小鼠的昏睡，但瘦素缺乏绕过了对NE的需求，因为DBL MUT小鼠在禁食时容易进入昏睡。这些数据表明，白色脂肪的交感神经激活和瘦素的抑制是小鼠麻痹发作所必需的。从麻木出现严重延迟DBL MUT小鼠，揭示了一种新的，瘦素独立的作用，NE在麻木恢复。通过在麻痹发作期间向对照小鼠施用β3肾上腺素能受体拮抗剂来模拟该表型。因此，通过棕色脂肪中的β3肾上腺素能受体的NE信号传导是第一个被鉴定为从麻木中正常恢复所需的神经递质-受体系统。
Some mammals, including laboratory mice, enter torpor in response to food deprivation, and leptin can attenuate these bouts of torpor. We previously showed that dopamine β-hydroxylase knockout (Dbh −/−) mice, which lack norepinephrine (NE), do not reduce circulating leptin upon fasting nor do they enter torpor. To test whether the onset of torpor in mice during a fast requires a NE-mediated reduction in circulating leptin, double mutant mice deficient in both leptin (ob/ob) and DBH (DBL MUT) were generated. Upon fasting, control and ob/ob mice entered torpor as assessed by telemetric core Tb acquisition. While fasting failed to induce torpor in Dbh −/− mice, leptin deficiency bypassed the requirement for NE, as DBL MUT mice readily entered torpor upon fasting. These data indicate that sympathetic activation of white fat and suppression of leptin is required for the onset of torpor in the mouse. Emergence from torpor was severely retarded in DBL MUT mice, revealing a novel, leptin-independent role for NE in torpor recovery. This phenotype was mimicked by administration of a β3 adrenergic receptor antagonist to control mice during a torpor bout. Hence, NE signaling via β3 adrenergic receptors presumably in brown fat is the first neurotransmitter-receptor system identified that is required for normal recovery from torpor.
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影响因子：
4.8
作者：
Golozoubova, V;Hohtola, E;Nedergaard, J
通讯作者：
Nedergaard, J
影响因子：
4.8
作者：
Brito, Marcia N.;Brito, Nilton A.;Bartness, Timothy J.
通讯作者：
Bartness, Timothy J.
DOI：
10.1086/physzool.52.2.30152564
发表时间：
1979-01-01
期刊：
PHYSIOLOGICAL ZOOLOGY
影响因子：
--
作者：
HUDSON, JW;SCOTT, IM
通讯作者：
SCOTT, IM
影响因子：
3.5
作者：
MORY, G;BOUILLAUD, F;RICQUIER, D
通讯作者：
RICQUIER, D
影响因子：
1.5
作者：
Rasmussen, AT
通讯作者：
Rasmussen, AT