Hypothalamic neurons - Mechanisms of sensitivity to temperature

Hypothalamic neurons - Mechanisms of sensitivity to temperature
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DOI:
10.1111/j.1749-6632.1998.tb08319.x
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发表时间:
1998-01-01
期刊:
MOLECULAR MECHANISMS OF FEVER
影响因子:
--
通讯作者:
Boulant, JA
Boulant, JA
中科院分区:
其他
文献类型:
--
作者:
Boulant, JA

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下丘脑吻端神经元受影响体温调节和发热的内源性因素的影响。细胞内记录揭示了负责神经元热敏性的突触和内在机制。许多温度敏感和温度不敏感神经元显示出先于动作电位的去极化前电位。温度对不敏感神经元的前电位几乎没有影响;然而,在温敏感神经元中,前电位的去极化因变暖而升高,这增加了放电频率。细胞内cAMP可以通过增强前电位的热反应来增加神经元的温度敏感性,最有可能是通过温度敏感的离子电导。温敏神经元也从温度不敏感神经元接收抑制性突触输入(IPSP),增强了一些神经元的热敏性,因为冷却增加了IPSP的幅度和持续时间。因此,即使IPSP频率不变,愚弄也可以通过增加IPSP振幅来降低放电频率。由于内源性因素改变神经元的放电率和热敏性,这些变化可能发生在突触后和突触前,以及通过离子电导确定动作电位之间的时间间隔。
Rostral hypothalamic neurons are influenced by endogenous factors that affect thermoregulation and fever. Intracellular recordings reveal the synaptic and intrinsic mechanisms responsible for neuronal thermosensitivity. Many temperature-sensitive and temperature-insensitive neurons display a depolarizing prepotential that precedes action potentials. Temperature has little effect on the prepotential of insensitive neurons; however, in warm-sensitive neurons, the prepotential's depolarization is elevated by warming, and this increases the firing rate. Intracellular cAMP can increase neuronal thermosensitivity by enhancing the thermal response of the prepotential, most likely by thermosensitive ionic conductances. Warm-sensitive neurons also receive inhibitory synaptic input (IPSPs) from temperature-insensitive neurons, enhancing the thermosensitivity of some neurons, because cooling increases IPSP amplitude and duration. Therefore, even though IPSP frequencies do not change, fooling can decrease firing rates by increasing IPSP amplitudes. Because endogenous factors change neuronal firing rate and thermosensitivity, these changes likely occur both post- and presynaptically as well as by ionic conductances that determine the time interval between action potentials.