Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia.
Centre for Neuroscience, College of Medicine and Public Health, Flinders University, Adelaide, SA, Australia.
Brain Res. 2020 Apr 1;1732:146678. doi: 10.1016/j.brainres.2020.146678. Epub 2020 Jan 22.
Emotionally significant stimuli, including potential threats from the external environment, trigger an increase in body temperature, a response known as emotional hyperthermia. Sympathetically-mediated brown adipose tissue (BAT) thermogenesis contributes substantially to this hyperthermic response. The systemic administration of α-adrenergic agonists is known to inhibit both febrile and shivering responses. In the present study, we investigated whether systemic administration of clonidine, a α-adrenoceptor agonist, attenuates the emotional hyperthermia evoked in conscious unrestrained rats suddenly confronted with a second (intruder) rat, itself confined to a small cage. Pre-implanted thermistors were used to measure BAT and body temperature in conscious, freely moving, male Sprague-Dawley rats. The rats were pre-treated with intraperitoneally administered vehicle (Ringer solution) or clonidine (1, 10 and 100 µg/kg). Clonidine, in a dose-dependent manner, reduced the intruder-elicited increases in BAT (log-dose linear regression F(1,16) = 9.52, R = 0.37, P < 0.01) and body temperature (F(1,16) = 6.48, R = 0.29, P < 0.05). We also investigated, in anesthetized rats, whether systemic clonidine administration inhibits BAT sympathetic nerve discharge evoked via activation of neurons in the lateral habenula (LHb) - a nucleus involved in the regulation of emotional hyperthermia. In anesthetized rats, clonidine abolished the BAT sympathetic nerve discharges elicited via bicuculline-mediated disinhibition of the LHb. These results suggest that activation of central α-adrenergic receptors attenuates the process of emotional hyperthermia by reduction of BAT thermogenesis.
情绪相关的刺激，包括来自外部环境的潜在威胁，会引发体温升高，这种反应被称为情绪性体温过高。交感神经介导的棕色脂肪组织（BAT）产热对这种体温过高反应有很大贡献。已知全身给予α-肾上腺素能激动剂可同时抑制发热和寒战反应。在本研究中，我们探讨了全身给予可乐定（一种α-肾上腺素受体激动剂）是否会减弱突然面对第二只（入侵者）大鼠的束缚自由活动的清醒大鼠的情绪性体温过高，而第二只大鼠本身被限制在一个小笼子里。预先植入的热敏电阻用于测量束缚自由活动的雄性 Sprague-Dawley 大鼠的 BAT 和体温。大鼠预先接受腹腔内给予载体（林格溶液）或可乐定（1、10 和 100µg/kg）处理。可乐定以剂量依赖性方式降低入侵者引起的 BAT（对数剂量线性回归 F(1,16) = 9.52，R = 0.37，P < 0.01）和体温（F(1,16) = 6.48，R = 0.29，P < 0.05）升高。我们还在麻醉大鼠中研究了全身给予可乐定是否通过抑制外侧缰核（LHb）中的神经元激活来抑制 BAT 交感神经放电，而 LHb 参与了情绪性体温过高的调节。在麻醉大鼠中，可乐定消除了通过双环己基脲介导的 LHb 去抑制引起的 BAT 交感神经放电。这些结果表明，通过减少 BAT 产热，中枢α-肾上腺素受体的激活减弱了情绪性体温过高的过程。
