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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• 作者：Claudia Fischer^a ; ^b ; ² ; Elmar Christ^a ; ² ; Horst-Werner Korf^a ; ^b ; ^{korf@em.uni-frankfurt.de} ; Charlotte von Gall^a ; ^b ; ¹
• 关键词：Pars tuberalis ; Hippocampus ; MT1 ; 7530404M11Riken ; Fam19a3
• 刊名：General and Comparative Endocrinology
• 出版年：2012
• 期刊代码：169_00166480
• 类别：bio
• 出版时间：15 May, 2012
• 卷：177
• 期：1
• 页码：98-103
• 文件大小：418 K

摘要

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 鈥渞etrograde鈥?pathway to the hypothalamus and via an 鈥渁nterograde鈥?pathway to the PD. TSH has been identified as 鈥渞etrograde鈥?messenger, while endocannabinoids function as messengers of the 鈥渁nterograde鈥?pathway. Here we show in mice that the PT expresses Tafa-3 encoding for a secretory peptide. In the PT 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 PT 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.