Preoptic bombesin-like receptor-3 neurons heat it up.
Preoptic bombesin-like receptor-3 neurons heat it up.
复制标题
视前铃蟾肽样受体 3 神经元将其加热。
DOI：
10.1080/23328940.2022.2047574
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
Reitman,MarcL
中科院分区：
文献类型：
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作者：
Piñol,RamónA;Reitman,MarcL
恒温动物（包括哺乳动物）的一个定义特征是温暖、高度调节和稳定的核心体温（Tb）。识别控制结核病的神经元网络对于理解这种基本生理学至关重要。视前区（POA）是接收传入和局部Tb感觉信息并容纳自主和行为体温调节通路的传出神经元的脑区[1]。这些通路有助于体温调节行为、寒战和非寒战产热、皮肤血管舒缩和心血管反应。研究人员已经确定了小鼠中的POA神经元群体，它们在激活时减少Tb，调节睡眠期间的热防御，麻木和体温调节。十几个这样的群体的特点是编码酶，神经肽和/或受体的基因的表达，主要是谷氨酸能。未来的研究将需要更好地描述这些异质神经元群体，揭示重叠，并定义具有更精确作用的亚群。已经提出了一种激活时增加Tb的POA群体，并且可能使用背内侧下丘脑（DMH）的丘脑能投射[2]。我们现在已经鉴定出表达蛙皮素样受体-3（POABRS3）的POA神经元作为第一个定义的特定群体，其激活增加Tb [3]。这是由棕色脂肪组织（BAT）激活的非颤抖性产热驱动的，伴随着心率和血压的增加。BRS 3是哺乳动物中的孤儿G蛋白偶联受体，尽管胃泌素释放肽和神经介肽B在其他一些脊椎动物中是内源性配体。Brs3在有限的下丘脑和其他脑区域以及一些外周细胞中表达。具有Brs3的生殖系消融的小鼠变得肥胖，并且具有较低的光相静息Tb和静息心率。在海马神经元中的Brs3的消融引起了与全球Brs3无效小鼠相似的肥胖和Tb表型，并且仅在海马神经元中的Brs3的再表达逆转了无效表型。因此，在谷氨酸能神经元发育期间和/或之后，BRS 3功能在调节Tb和能量稳态的其他方面具有作用。
A defining characteristic of endotherms, including mammals, is a warm, highly regulated, and stable core body temperature (Tb). Identifying the network of neurons controlling Tb is essential for understanding this fundamental physiology. The preoptic area (POA) is a brain region that receives afferent and local Tb sensory information and harbors efferent neurons of autonomic and behavioral thermoregulatory pathways [1]. These pathways contribute to thermoregulatory behavior, shivering and non-shivering thermogenesis, cutaneous vasomotion and cardiovascular responses. Researchers have identified POA neuronal populations in mice that reduce Tb when activated, regulating heat defense, torpor, and thermoregulation during sleep. A dozen such populations are marked by the expression of genes encoding enzymes, neuropeptides, and/or receptors and are predominantly glutamatergic. Future studies will need to better characterize these heterogenous neuronal populations, uncovering overlaps and defining subpopulations with more precise roles. A POA population that increases Tb when activated has been proposed and likely uses glutamatergic projections to the dorsomedial hypothalamus (DMH)[2]. We have now identified POA neurons expressing bombesin-like receptor-3 (POABRS3) as the first defined, specific population whose activation increases Tb [3]. This is driven by nonshivering thermogenesis through brown adipose tissue (BAT) activation, with concomitant increases in heart rate and blood pressure.BRS3 is an orphan G protein-coupled receptor in mammals, although both gastrin-releasing peptide and neuromedin B are endogenous ligands in some other vertebrates. Brs3 is expressed in limited hypothalamic and other brain regions and in some peripheral cells. Mice with germline ablation of Brs3 become obese and have a lower light phase resting Tb and resting heart rate. Ablation of Brs3 in glutamatergic neurons caused a similar obesity and Tb phenotype as the global Brs3 null mice, and reexpression of Brs3 only in glutamatergic neurons reversed the null phenotype. Thus, BRS3 function, during and/or after glutamatergic neuronal development, has a role in regulating Tb and other aspects of energy homeostasis.