The effects of Cirazoline, an alpha-1 adrenoreceptor agonist, on the firing rates of thermally classified anterior hypothalamic neurons in rat brain slices.

The effects of Cirazoline, an alpha-1 adrenoreceptor agonist, on the firing rates of thermally classified anterior hypothalamic neurons in rat brain slices.
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西拉唑啉(一种 α-1 肾上腺素受体激动剂)对大鼠脑切片中热分类下丘脑前神经元放电率的影响。

DOI:
10.1016/j.brainres.2007.12.016
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发表时间:
2008
期刊:
影响因子:
2.9
通讯作者:
Griffin,JohnD
Griffin,JohnD
中科院分区:
医学3区
文献类型:
--
作者:
Imbery,TedE;Irdmusa,MitraS;Speidell,AndrewP;Streer,MarkS;Griffin,JohnD

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外周接触 LPS 会诱发双相发热,这种发热被认为是通过迷走神经传入下丘脑前部 (POAH) 的视前区引发的,POAH 是大脑中重要的体温调节控制中心。先前的研究表明,去甲肾上腺素通过选择性激活 α2 肾上腺素受体 (AR),突触介导这种前列腺素 E2 (PGE2) 依赖性温度变化。然而,有明确的证据表明,下丘脑温度调节神经元的 α-1 AR 激活将导致不依赖于 PGE2 的快速高温。本研究通过记录成年雄性大鼠组织切片中 POAH 神经元对温度和选择性 α-1 AR 激动剂西拉唑啉 (1–100 μM) 的反应,测试了去甲肾上腺素在 POAH 中的直接作用。神经元被分为热敏感型或温度不敏感型。温敏感神经元对西拉唑林的反应是放电率降低,而温度不敏感神经元则显示放电率增加。这些反应与报道的 PGE2 反应相似,表明 POAH 中的热敏感和温度不敏感神经元在调节这种 α-1 AR 依赖性体温过高转变中都很重要。
Peripheral exposure to LPS induces a biphasic fever thought to be initiated via vagal afferents to the preoptic area of the anterior hypothalamus (POAH), an important thermoregulatory control center in the brain. Previous studies have shown that norepinephrine synaptically mediates this Prostaglandin E2(PGE2)-dependent change in temperature through the selective activation of alpha-2 adrenoreceptors (AR). However, there is clear evidence that alpha-1 AR activation of thermoregulatory hypothalamic neurons will result in a rapid hyperthermia that is not dependent on PGE2. This direct action of norepinephrine in the POAH was tested in the present study by recording the single-unit activity of POAH neurons in a tissue slice preparation from the adult male rat, in response to temperature and the selective alpha-1 AR agonist Cirazoline (1–100 μM). Neurons were classified as either warm sensitive or temperature insensitive. Warm sensitive neurons responded to Cirazoline with a decrease in firing rate, while temperature insensitive neurons showed a firing rate increase. These responses are similar to those reported for PGE2and suggest that both warm sensitive and temperature insensitive neurons in the POAH are important in mediating this alpha-1 AR-dependent hyperthermic shift in body temperature.
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