Repeated Cold Stress Enhances the Acute Restraint Stress-Induced Hyperthermia in Mice
Repeated Cold Stress Enhances the Acute Restraint Stress-Induced Hyperthermia in Mice
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DOI：
10.1248/bpb.b16-00343
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发表时间：
2017-01-01
影响因子：
2
通讯作者：
Kawabata, Atsufumi
中科院分区：
文献类型：
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作者：
Miyamoto, Tomoyoshi;Funakami, Yoshinori;Kawabata, Atsufumi
根据特定的时间表（称为特定温度节律交替（SART）），啮齿类动物会表现出自主神经失衡，现在被用作纤维肌痛的实验模型。为了探讨 SART 应激动物对新型急性应激的敏感性，我们测试了小鼠暴露于 SART 应激 1 周是否会改变急性束缚应激诱导的高热程度。小鼠接受 7 天的 SART 应激训练；即，白天（09:00-16:00）将小鼠以1小时的间隔交替暴露于24°C和4°C，并在4°C下过夜（16:00-09:00）。 SART应激和未应激小鼠均受到急性束缚应激20-60分钟，在此期间监测直肠温度。在受到束缚压力 60 分钟之前和之后测量血清皮质酮水平。 SART 应激本身不会改变小鼠的体温或血清皮质酮水平。急性束缚应激会增加体温和血清皮质酮水平，这两种反应在 SART 应激小鼠中都比未应激小鼠更强。 SR59230A（一种 β（3）肾上腺素受体拮抗剂）显着减弱了 SART 应激小鼠对急性约束应激的增强热反应，但不受地西泮（一种抗焦虑药）、米非司酮（一种糖皮质激素受体拮抗剂）或吲哚美辛（一种环氧合酶抑制剂）的影响。这些结果表明，SART应激增强了小鼠对急性约束应激的敏感性，其特征是过热和皮质酮分泌增加，并且对急性应激的过热反应增加可能涉及交感β（3）肾上腺素受体的加速激活，已知该受体可调节棕色脂肪组织中的非颤抖产热作用。
The rodents exposed to repeated cold stress according to a specific schedule, known as specific alternation of rhythm in temperature (SART), exhibit autonomic imbalance, and is now used as an experimental model of fibromyalgia. To explore the susceptibility of SART-stressed animals to novel acute stress, we tested whether exposure of mice to SART stress for 1 week alters the extent of acute restraint stress-induced hyperthermia. Mice were subjected to 7-d SART stress sessions; i.e., the mice were alternately exposed to 24 and 4 degrees C at 1-h intervals during the daytime (09:00-16:00) and kept at 4 degrees C overnight (16:00-09:00). SART-stressed and unstressed mice were exposed to acute restraint stress for 20-60 min, during which rectal temperature was monitored. Serum corticosterone levels were measured before and after 60-min exposure to restraint stress. SART stress itself did not alter the body temperature or serum corticosterone levels in mice. Acute restraint stress increased the body temperature and serum corticosterone levels, both responses being greater in SART-stressed mice than unstressed mice. The enhanced hyperthermic responses to acute restraint stress in SART-stressed mice were significantly attenuated by SR59230A, a beta(3) adrenoceptor antagonist, but unaffected by diazepam, an anxiolytic, mifepristone, a glucocorticoid receptor antagonist, or indomethacin, a cyclooxygenase inhibitor. These results suggest that SART stress enhances the susceptibility of mice to acute restraint stress, characterized by increased hyperthermia and corticosterone secretion, and that the increased hyperthermic responses to acute stress might involve accelerated activation of sympathetic beta(3) adrenoceptors, known to regulate non-shivering thermogenesis in the brown adipose tissue.