Tafa-3 encoding for a secretory peptide is expressed in the mouse pars tuberalis and is affected by melatonin 1 receptor deficiency
Tafa-3 encoding for a secretory peptide is expressed in the mouse pars tuberalis and is affected by melatonin 1 receptor deficiency
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DOI：
10.1016/j.ygcen.2012.02.016
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发表时间：
2012-05-15
影响因子：
2.7
通讯作者：
von Gall, Charlotte
中科院分区：
文献类型：
--
作者：
Fischer, Claudia;Christ, Elmar;von Gall, Charlotte
垂体结节部（PT）是垂体前叶（PD）与神经内分泌中枢（下丘脑、松果体）之间的重要界面。最好的研究作用的PT是控制季节性变化的功能。在哺乳动物中，从松果体分泌的褪黑激素代表PT的主要输入信号。通过作用于褪黑激素1型受体（MT 1），褪黑激素控制PT的功能活性。最有趣的是，PT在两个方向上发送其输出信号：通过“逆行”途径到达下丘脑，并通过“顺行”途径到达PD。促甲状腺激素已被确定为“逆行”信使，而内源性大麻素的功能作为信使的“顺行”途径。在这里，我们表明在小鼠中，PT表达Tafa-3编码的分泌肽。在野生型小鼠的FT中，Tafa-3 mRNA水平在白天和夜晚之间变化：它们在中午低，在午夜高。在具有MT 1受体的靶向缺失的小鼠的FIT中没有观察到这种日/夜差异，表明PT中的Tafa-3 mRNA表达由通过MT 1受体起作用的褪黑激素控制。值得注意的是，Tafa-3表达不限于PT，但也发现在其他脑区，如海马，缰核和丘脑核。在这些区域，Tafa-3表达没有表现出昼夜差异，并且不受MT 1缺陷的影响。因此，Tafa-3的表达似乎是由区域特异性机制控制的。我们的数据表明，TAFA-3是一种来自PT的信号分子，并为新出现的概念提供了进一步的证据，即PT不是依赖于高度器官特异性的信使，而是采用了一种在其他大脑系统中也起作用的信号分子的混合物。(C)2012 Elsevier Inc. All rights reserved.
The hypophysial pars tuberalis (PT) is an important interface between neuroendocrine brain centers (hypothalamus, pineal organ) and the anterior lobe of the hypophysis (PD). The best investigated role of the PT is the control of seasonally changing functions. In mammals, melatonin secreted from the pineal organ represents a major input signal to the PT. By acting upon melatonin type 1 receptors (MT1) melatonin controls the functional activity of the PT. Most interestingly, the PT sends its output signals in two directions: via a "retrograde" pathway to the hypothalamus and via an "anterograde" pathway to the PD. TSH has been identified as "retrograde" messenger, while endocannabinoids function as messengers of the "anterograde" pathway. Here we show in mice that the PT expresses Tafa-3 encoding for a secretory peptide. In the FT of wild type mice Tafa-3 mRNA levels varied between day and night: they were low at mid-day and high at mid-night. This day/night difference was not observed in the FIT of mice with a targeted deletion of the MT1 receptor indicating that Tafa-3 mRNA expression in the PT is controlled by melatonin acting through the MT1 receptor. Notably, Tafa-3 expression was not restricted to the PT, but was also found in other brain regions, such as the hippocampus, the habenular and thalamic nuclei. In these regions, Tafa-3 expression did not display a day/night difference and was not affected by MT1-deficiency. Thus, Tafa-3 expression appears to be controlled by region-specific mechanisms. Our data suggest that TAFA-3 is a signaling molecule from the PT and provides further evidence for the emerging concept that the PT rather than relying upon highly organ-specific messengers employs a cocktail of signaling molecules that also operate in other brain systems. (C) 2012 Elsevier Inc. All rights reserved.