Kalliomäki M-L, Panula P
Neuroscience Center and Institute of Biomedicine/Anatomy, Biomedicum Helsinki, University of Helsinki, Finland.
Neuroscience. 2004;124(1):81-7. doi: 10.1016/j.neuroscience.2003.10.026.
Hypothalamic paraventricular and supraoptic nuclei are involved in the body fluid homeostasis. Especially vasopressin peptide and mRNA levels are regulated by hypo- and hyperosmolar stimuli. Other neuropeptides such as dynorphin, galanin and neuropeptide FF are coregulated with vasopressin. In this study neuropeptide FF and another RF-amide peptide, the prolactin-releasing peptide mRNA levels were studied by quantitative in situ hybridization after chronic salt loading, a laboratory model of chronic dehydration. The neuropeptide FF mRNA expressing cells virtually disappeared from the hypothalamic supraoptic and paraventricular nuclei after salt loading, suggesting that hyperosmolar stress downregulated the NPFF gene transcription. The neuropeptide FF mRNA signal levels were returned to control levels after the rehydration period of 7 days. No changes were observed in those medullary nuclei that express neuropeptide FF mRNA. No significant changes were observed in the hypothalamic or medullary prolactin-releasing peptide mRNA levels. Neuropeptide FF mRNA is drastically downregulated in the hypothalamic magnocellular neurons after salt loading. Other neuropeptides studied in this model are concomitantly coregulated with vasopressin: i.e. their peptide levels are downregulated and mRNA levels are upregulated which is in contrast to neuropeptide FF regulation. It can thus be concluded that neuropeptide FF is not regulated through the vasopressin regulatory system but via an independent pathway. The detailed mechanisms underlying the downregulation of neuropeptide FF mRNA in neurons remain to be clarified.
下丘脑室旁核和视上核参与体液平衡的调节。尤其是血管升压素肽和mRNA水平受低渗和高渗刺激的调节。强啡肽、甘丙肽和神经肽FF等其他神经肽与血管升压素共同调节。在本研究中,采用慢性脱水的实验室模型——慢性盐负荷后,通过定量原位杂交技术研究了神经肽FF和另一种RF酰胺肽——催乳素释放肽的mRNA水平。盐负荷后,表达神经肽FF mRNA的细胞几乎从下丘脑视上核和室旁核消失,提示高渗应激下调了NPFF基因转录。7天的补液期后,神经肽FF mRNA信号水平恢复到对照水平。在表达神经肽FF mRNA的髓质核中未观察到变化。下丘脑或髓质催乳素释放肽mRNA水平未观察到显著变化。盐负荷后,下丘脑大细胞神经元中的神经肽FF mRNA显著下调。本模型中研究的其他神经肽与血管升压素共同调节:即它们的肽水平下调而mRNA水平上调,这与神经肽FF的调节相反。因此可以得出结论,神经肽FF不是通过血管升压素调节系统调节,而是通过独立途径调节。神经元中神经肽FF mRNA下调的详细机制仍有待阐明。