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调节皮肤血流和出汗的传出体温调节通路。

Efferent thermoregulatory pathways regulating cutaneous blood flow and sweating.

作者信息

McAllen Robin M, McKinley Michael J

机构信息

Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, Australia.

Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, Australia; Department of Physiology, University of Melbourne, Parkville, VIC, Australia.

出版信息

Handb Clin Neurol. 2018;156:305-316. doi: 10.1016/B978-0-444-63912-7.00018-7.

Abstract

Cutaneous vasoconstrictor nerves regulate heat retention, and are activated by falls in skin or core temperature. The efferent pathways controlling this process originate within the preoptic area. A descending GABAergic pathway, activated by warm skin or core, indirectly inhibits sympathetic premotor neurons in the medullary raphé. Those premotor neurons drive cutaneous vasoconstriction via excitatory glutamatergic and serotonergic connections to spinal preganglionic neurons. Cold skin and/or cold core temperatures activate a direct preoptic-to-raphé excitatory pathway. The balance of inhibitory and excitatory influences reaching the medullary raphé determines cutaneous blood flow. During fever, prostaglandin E inhibits preoptic GABAergic neurons, resulting in disinhibition of the excitatory preoptic-to-raphé pathway, and hence, cutaneous vasoconstriction. A weaker, parallel source of descending excitatory drive reaches cutaneous preganglionic neurons from the rostral ventrolateral medulla. Sweating follows local heating of the preoptic area in cats and monkeys, and heated humans show sweating-related activation of this same region in functional magnetic resonance imaging (fMRI) studies. A descending pathway that drives sweating has been traced in cats from the hypothalamus to putative premotor neurons in the parafacial region at the pontomedullary junction. The homologous parafacial region in humans also shows sweating-related activation in fMRI studies. The central pathways that drive active vasodilatation in human nonacral skin remain unknown.

摘要

皮肤血管收缩神经调节热量保留,并在皮肤或核心体温下降时被激活。控制这一过程的传出通路起源于视前区。一条下行的γ-氨基丁酸能通路,在皮肤或核心体温升高时被激活,间接抑制延髓中缝的交感运动前神经元。这些运动前神经元通过与脊髓节前神经元的兴奋性谷氨酸能和5-羟色胺能连接来驱动皮肤血管收缩。皮肤寒冷和/或核心体温降低会激活一条从视前区直接到中缝的兴奋性通路。到达延髓中缝的抑制性和兴奋性影响的平衡决定了皮肤血流量。在发热期间,前列腺素E抑制视前区的γ-氨基丁酸能神经元,导致对视前区到中缝的兴奋性通路的去抑制,从而引起皮肤血管收缩。一个较弱的、平行的下行兴奋性驱动源从延髓头端腹外侧到达皮肤节前神经元。在猫和猴子中,视前区局部受热会引发出汗,功能性磁共振成像(fMRI)研究表明,受热的人类在同一区域会出现与出汗相关的激活。在猫中,已经追踪到一条从下丘脑到脑桥延髓交界处旁面部区域假定的运动前神经元的下行通路,该通路驱动出汗。fMRI研究表明,人类的同源旁面部区域在出汗时也会被激活。驱动人类非手足皮肤主动血管舒张的中枢通路仍然未知。

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