Hypothermia in mouse is caused by adenosine A(1) and A(3) receptor agonists and AMP via three distinct mechanisms.
Hypothermia in mouse is caused by adenosine A(1) and A(3) receptor agonists and AMP via three distinct mechanisms.
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DOI：
10.1016/j.neuropharm.2016.11.026
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发表时间：
2017-03-01
影响因子：
4.7
通讯作者：
Reitman ML
中科院分区：
文献类型：
--
作者：
Carlin JL;Jain S;Gizewski E;Wan TC;Tosh DK;Xiao C;Auchampach JA;Jacobson KA;Gavrilova O;Reitman ML
小型哺乳动物有能力进入休眠状态，这是一种体温过低、代谢低下的状态，可以节省大量能量。给予腺苷或腺苷 5'-单磷酸 (AMP) 可以引发体温过低、类似麻木的状态。我们通过遥测监测野生型和受体敲除小鼠（Adora1−/−、Adora3−/−）小鼠的体温来研究体温过低的机制。证实之前的数据，刺激 A3 腺苷受体 (AR) 通过外周肥大细胞脱颗粒、组胺释放和中枢组胺 H1 受体激活诱导体温降低。相比之下，A1AR 激动剂和 AMP 均起中枢作用，导致体温过低。常用的选择性 A1AR 激动剂，包括 N6-环戊基腺苷 (CPA)、N6-环己基腺苷 (CHA) 和 MRS5474，腹腔内给药时可通过 A1AR 和 A3AR 引起体温过低。脑室内给药、低外周剂量的 Cl-ENBA [(±)-5'-氯-5'-脱氧-N6-内-降冰片腺苷]或使用 Adora3−/− 小鼠可以选择性刺激 A1AR。 AMP 刺激的低温可以独立于 A1AR、A3AR 和肥大细胞发生。 A1AR 和 A3AR 激动剂和 AMP 会引起调节性体温过低，其特征是总能量消耗下降、身体缺乏活动以及偏好较冷的环境温度，这表明体温设定点降低。 A1AR 和 A3AR 都不是禁食引起的麻木状态所必需的。 A1AR 和 A3AR 激动剂以及 AMP 通过三种不同的机制触发调节性低温。
Small mammals have the ability to enter torpor, a hypothermic, hypometabolic state, allowing impressive energy conservation. Administration of adenosine or adenosine 5'-monophosphate (AMP) can trigger a hypothermic, torpor-like state. We investigated the mechanisms for hypothermia using telemetric monitoring of body temperature in wild type and receptor knock out (Adora1−/−, Adora3−/−) mice. Confirming prior data, stimulation of the A3 adenosine receptor (AR) induced hypothermia via peripheral mast cell degranulation, histamine release, and activation of central histamine H1 receptors. In contrast, A1AR agonists and AMP both acted centrally to cause hypothermia. Commonly used, selective A1AR agonists, including N6-cyclopentyladenosine (CPA), N6-cyclohexyladenosine (CHA), and MRS5474, caused hypothermia via both A1AR and A3AR when given intraperitoneally. Intracerebroventricular dosing, low peripheral doses of Cl-ENBA [(±)-5'-chloro-5'-deoxy-N6-endo-norbornyladenosine], or using Adora3−/− mice allowed selective stimulation of A1AR. AMP-stimulated hypothermia can occur independently of A1AR, A3AR, and mast cells. A1AR and A3AR agonists and AMP cause regulated hypothermia that was characterized by a drop in total energy expenditure, physical inactivity, and preference for cooler environmental temperatures, indicating a reduced body temperature set point. Neither A1AR nor A3AR were required for fasting-induced torpor. A1AR and A3AR agonists and AMP trigger regulated hypothermia via three distinct mechanisms.
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影响因子：
7.3
作者：
Franchetti, Palmarisa;Cappellacci, Loredana;Grifantini, Mario
通讯作者：
Grifantini, Mario
影响因子：
4.8
作者：
Daniels, Isadora Susan;Zhang, Jianfa;Lee, Cheng Chi
通讯作者：
Lee, Cheng Chi
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
DOI：
10.1073/pnas.92.10.4666
发表时间：
1995-05-09
影响因子：
11.1
作者：
HEURTEAUX, C;LAURITZEN, I;LAZDUNSKI, M
通讯作者：
LAZDUNSKI, M
DOI：
10.4161/23328940.2014.976512
发表时间：
2015-04
期刊：
Temperature (Austin, Tex.)
影响因子：
--
作者：
Drew KL;Romanovsky AA;Stephen TK;Tupone D;Williams RH
通讯作者：
Williams RH