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研究揭示抑制钠食欲的神经基础
作者:小柯机器人 发布时间:2020/1/23 16:29:06

韩国科学技术院Jong-Woo Sohn、美国德克萨斯大学西南医学中心Chen Liu等研究人员合作揭示抑制钠食欲的神经基础。相关论文2020年1月20日在线发表于国际学术期刊《自然—神经科学》。

研究人员发现,在臂外侧臂旁核中表达5-羟色胺2c受体(Htr2c)的神经元(LPBNHtr2c神经元)抑制食欲。这些神经元的活动由体内钠含量所调节,它们的激活可以迅速抑制钠的摄入。相反,即使在正常情况下,对这些神经元的抑制也会特异性地促进钠食欲。值得注意的是,LPBN神经元表达的Htr2c的生理作用是抑制食欲。这些研究结果表明,LPBNHtr2c神经元可作为抵抗钠食欲的刹车角色,并且需要缓解它们才能充分体现钠食欲。

据悉,钠食欲是一种强有力的动机,可以促使缺钠的动物摄入大量而又厌恶的钠。但是,在正常情况下,钠食欲会受到抑制,以防止体内稳态偏差。尽管最近刺激食欲钠的分子和神经机制受到了广泛关注,但抑制食欲钠的机制仍然不甚明确。

附:英文原文

Title: A neural basis for tonic suppression of sodium appetite

Author: Seahyung Park, Kevin W. Williams, Chen Liu, Jong-Woo Sohn

Issue&Volume: 2020-01-20

Abstract: Sodium appetite is a powerful form of motivation that can drive ingestion of high, yet aversive concentrations of sodium in animals that are depleted of sodium. However, in normal conditions, sodium appetite is suppressed to prevent homeostatic deviations. Although molecular and neural mechanisms underlying the stimulation of sodium appetite have received much attention recently, mechanisms that inhibit sodium appetite remain largely obscure. Here we report that serotonin 2c receptor (Htr2c)-expressing neurons in the lateral parabrachial nucleus (LPBNHtr2c neurons) inhibit sodium appetite. Activity of these neurons is regulated by bodily sodium content, and their activation can rapidly suppress sodium intake. Conversely, inhibition of these neurons specifically drives sodium appetite, even during euvolemic conditions. Notably, the physiological role of Htr2c expressed by LPBN neurons is to disinhibit sodium appetite. Our results suggest that LPBNHtr2c neurons act as a brake against sodium appetite and that their alleviation is required for the full manifestation of sodium appetite.

DOI: 10.1038/s41593-019-0573-2

Source: https://www.nature.com/articles/s41593-019-0573-2

期刊信息

Nature Neuroscience:《自然—神经科学》,创刊于1998年。隶属于施普林格·自然出版集团,最新if:21.126
官方网址:https://www.nature.com/neuro/
投稿链接:https://mts-nn.nature.com/cgi-bin/main.plex