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下丘脑神经元。对温度的敏感机制。

Hypothalamic neurons. Mechanisms of sensitivity to temperature.

作者信息

Boulant J A

机构信息

Department of Physiology, College of Medicine, The Ohio State University, Columbus, Ohio 43210, USA.

出版信息

Ann N Y Acad Sci. 1998 Sep 29;856:108-115. doi: 10.1111/j.1749-6632.1998.tb08319.x.

Abstract

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, cooling 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.

摘要

下丘脑前部神经元受影响体温调节和发热的内源性因素影响。细胞内记录揭示了神经元热敏感性的突触和内在机制。许多温度敏感和温度不敏感的神经元在动作电位之前会出现去极化预电位。温度对不敏感神经元的预电位影响很小;然而,在温度敏感神经元中,预电位的去极化会因升温而增强,这会增加放电频率。细胞内的环磷酸腺苷(cAMP)可通过增强预电位的热反应来增加神经元的热敏感性,最有可能是通过热敏离子电导来实现。温度敏感神经元还从温度不敏感神经元接收抑制性突触输入(抑制性突触后电位),这增强了一些神经元的热敏感性,因为冷却会增加抑制性突触后电位的幅度和持续时间。因此,即使抑制性突触后电位的频率不变,冷却也可通过增加抑制性突触后电位的幅度来降低放电频率。由于内源性因素会改变神经元的放电频率和热敏感性,这些变化可能在突触后和突触前以及通过决定动作电位时间间隔的离子电导发生。

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