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首页> 外文期刊>Progress in brain research >The TRH neuron: a hypothalamic integrator of energy metabolism.
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The TRH neuron: a hypothalamic integrator of energy metabolism.

机译：TRH神经元：下丘脑能量代谢的积分器。

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摘要

Thyrotropin-releasing hormone (TRH) has an important role in the regulation of energy homeostasis not only through effects on thyroid function orchestrated through hypophysiotropic neurons in the hypothalamic paraventricular nucleus (PVN), but also through central effects on feeding behavior, thermogenesis, locomotor activation and autonomic regulation. Hypophysiotropic TRH neurons are located in the medial and periventricular parvocellular subdivisions of the PVN and receive direct monosynaptic projections from two, separate, populations of leptin-responsive neurons in the hypothalamic arcuate nucleus containing either alpha-melanocyte-stimulating hormone (alpha-MSH) and cocaine- and amphetamine-regulated transcript (CART), peptides that promote weight loss and increase energy expenditure, or neuropeptide Y (NPY) and agouti-related protein (AGRP), peptides that promote weight gain and reduce energy expenditure. During fasting, the reduction in TRH mRNA in hypophysiotropic neurons mediated by suppression of alpha-MSH/CART simultaneously with an increase in NPY/AGRP gene expression in arcuate nucleus neurons contributes to the fall in circulating thyroid hormone levels, presumably by increasing the sensitivity of the TRH gene to negative feedback inhibition by thyroid hormone. Endotoxin administration, however, has the paradoxical effect of increasing circulating levels of leptin and melanocortin signaling and CART gene expression in arcuate nucleus neurons, but inhibiting TRH gene expression in hypophysiotropic neurons. This may be explained by an overriding inhibitory effect of endotoxin to increase type 2 iodothyroine deiodinase (D2) in a population of specialized glial cells, tanycytes, located in the base and infralateral walls of the third ventricle. By increasing the conversion of T4 into T3, tanycytes may increase local tissue concenetrations of thyroid hormone, and thereby induce a state of local tissue hyperthyroidism in the region of hypophysisotrophic TRH neurons. Other regions of the brain may also serve as metabolic sensors for hypophysiostropic TRH neurons including the ventrolateral medulla and dorsomedial nucleus of the hypothalamus that have direct monosynaptic projections to the PVN. TRH also exerts a number of effects within the central nervous system that may contribute to the regulation of energy homeostasis. Included are an increase in core body temperature mediated through neurons in the anterior hypothalamic-preoptic area that coordinate a variety of autonomic responses; arousal and locomotor activation through cholinergic and dopaminergic mechanisms on the septum and nucleus accumbens, respectively; and regulation of the cephalic phase of digestion. While the latter responses are largely mediated through cholinergic mechanisms via TRH neurons in the brainstem medullary raphe and dorsal motor nucleus of the vagus, effects of TRH on autonomic loci in the hypothalamic PVN may also be important. Contrary to the actions of T3 to increase appetite, TRH has central effects to reducefood intake in normal, fasting and stressed animals. The precise locus where TRH mediates this response is unknown. However, evidence that an anatomically separate population of nonhypophysiotropic TRH neurons in the anterior parvocellular subdivision of the PVN is integrated into the leptin regulatory control system by the same arcuate nucleus neuronal populations that innervate hypophysiotropic TRH neurons, raises the possibility that anterior parvocellular TRH neurons may be involved, possibly through interactions with the limbic nervous system.
机译：促甲状腺激素释放激素（TRH）在调节能量稳态中起着重要作用，不仅通过下丘脑室旁核（PVN）中的促体质神经元对甲状腺功能的影响，而且还通过对进食行为，生热，运动活动的中枢作用和自主调节。促体生长激素TRH神经元位于PVN的内侧和脑室小细胞细分中，并从下丘脑弓状核中两个单独的瘦素反应性神经元群体接受直接的单突触投射，这些神经元包含α-黑素细胞刺激激素（α-MSH）和可卡因和苯丙胺调节的转录物（CART），促进体重减轻并增加能量消耗的肽，或神经肽Y（NPY）和刺骨相关蛋白（AGRP），促进体重增加并减少能量消耗的肽。禁食期间，通过抑制α-MSH/ CART介导的促体垂体神经元TRH mRNA的减少，同时弓形核神经元中NPY / AGRP基因表达的增加，也有助于循环甲状腺激素水平的下降，大概是通过增加TRH基因对甲状腺激素的负反馈抑制作用。但是，内毒素给药具有悖论性的作用，即增加弓形核神经元中瘦素和黑皮质素信号传导和CART基因表达的循环水平，但抑制垂体神经元中TRH基因的表达。这可能是由于内毒素对位于第三脑室底壁和后壁的专门神经胶质细胞（单核细胞）群体中增加2型碘甲状腺素脱碘酶（D2）的抑制作用所致。通过增加T4到​​T3的转化，单核细胞可增加甲状腺激素的局部组织聚集，从而在体下营养TRH神经元区域诱发局部组织甲状腺功能亢进的状态。大脑的其他区域也可以用作低体力TRH神经元的代谢传感器，包括下丘脑的腹侧延髓和背核，它们的单突触投射直接指向PVN。 TRH还在中枢神经系统内发挥多种作用，可能有助于调节能量稳态。包括通过下丘脑前视区的神经元介导的核心体温的升高，这些神经元协调了各种自主神经反应。分别通过中隔和伏隔核的胆碱能和多巴胺能机制引起觉醒和运动激活;和消化的头相调节。虽然后者的反应很大程度上是通过脑干髓ra和迷走神经背运动核内TRH神经元通过胆碱能机制介导的，但TRH对下丘脑PVN中自主神经基因座的影响也可能很重要。与T3增强食欲的作用相反，TRH具有减少正常，禁食和压力大动物食物摄入的重要作用。 TRH介导此反应的确切基因座是未知的。但是，有证据表明，神经支配垂体性TRH神经元的弓形核神经元群体将PVN前小叶细小区内的解剖上分离的非低亲和性TRH神经元整合到了瘦素调节控制系统中，这增加了前小细胞TRH神经元可能可能通过与边缘神经系统的相互作用而参与进来​​。

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