Imaki T, Katsumata H, Konishi S-I, Kasagi Y, Minami S
Department of Bioregulation, Institute of Development and Ageing Sciences, Nippon Medical School, Graduate School, Kawasaki, Japan.
J Neuroendocrinol. 2003 Oct;15(10):916-24. doi: 10.1046/j.1365-2826.2003.01071.x.
In rats, acute stress substantially increases corticotropin-releasing factor (CRF) type 1 receptor (CRFR-1) mRNA expression in the paraventricular nucleus (PVN) and osmotic stimulation induces both CRF and CRFR-1 mRNA in magnocellular PVN and supraoptic nucleus (SON). However, these phenomena have not been analysed in other species. We compared CRF and CRFR-1 expression in rat and mouse hypothalamus. Male C57BL/6 mice and Wistar rats were exposed to acute restraint stress for 3 h, or to hypertonic saline ingestion for 7 days. Restraint stress increased CRF and c-fos mRNA expression in both rat and mouse PVN. CRFR-1 mRNA was barely detectable in controls, whereas restraint stress substantially increased CRFR-1 mRNA in rat PVN, but not in mouse. Hypertonic saline ingestion induced CRF mRNA in magnocellular PVN and SON of the rat, but did not alter CRF mRNA levels in mouse hypothalamus. CRFR-1 mRNA was also induced in magnocellular PVN and SON of the rat in response to osmotic stimulation, but not in mouse. Immunohistochemistry demonstrated that CRFR-1-like immunoreactivity (ir) was distributed within parvocellular and magnocellular PVN of mouse and rat. CRFR-1-ir in rat PVN was increased by acute stress and osmotic stimulation. By contrast, these treatments did not alter CRFR-1-ir in mouse PVN. Combined immunohistochemistry and in situ hybridization revealed that CRFR-1-ir was most frequently colocalized to CRF in mouse PVN, whereas only a small percentage of oxytocin and vasopressin-producing cells coexpressed CRFR-1-ir. These results indicate that (i) by contrast to rats, neither acute stress nor osmotic stimulation induces CRFR-1 mRNA expression in the mouse PVN; (ii) osmotic stimulation does not alter CRF mRNA expression in parvocellular and magnocellular neurones of mouse PVN; and (iii) acute stress increases c-fos and CRF mRNA to a similar degree in mouse and rat PVN. Thus, differences may exist between mouse and rat in the regulation of CRF and CRFR-1 gene expression in hypothalamus following stress and osmotic stimulation.
在大鼠中，急性应激可显著增加室旁核（PVN）中促肾上腺皮质激素释放因子（CRF）1型受体（CRFR-1）的mRNA表达，渗透刺激可诱导大细胞PVN和视上核（SON）中的CRF和CRFR-1 mRNA表达。然而，这些现象尚未在其他物种中进行分析。我们比较了大鼠和小鼠下丘脑CRF和CRFR-1的表达。将雄性C57BL/6小鼠和Wistar大鼠暴露于急性束缚应激3小时，或给予高渗盐水饮用7天。束缚应激增加了大鼠和小鼠PVN中CRF和c-fos mRNA的表达。对照组中几乎检测不到CRFR-1 mRNA，而束缚应激使大鼠PVN中的CRFR-1 mRNA显著增加，但小鼠中未增加。饮用高渗盐水可诱导大鼠大细胞PVN和SON中的CRF mRNA，但不改变小鼠下丘脑的CRF mRNA水平。渗透刺激也可诱导大鼠大细胞PVN和SON中的CRFR-1 mRNA，但小鼠中未诱导。免疫组织化学显示，CRFR-1样免疫反应性（ir）分布在小鼠和大鼠的小细胞和大细胞PVN内。急性应激和渗透刺激可增加大鼠PVN中的CRFR-1-ir。相比之下，这些处理并未改变小鼠PVN中的CRFR-1-ir。免疫组织化学和原位杂交相结合显示，在小鼠PVN中，CRFR-1-ir最常与CRF共定位，而只有一小部分产生催产素和加压素的细胞共表达CRFR-1-ir。这些结果表明：（i）与大鼠不同，急性应激和渗透刺激均不会诱导小鼠PVN中CRFR-1 mRNA的表达；（ii）渗透刺激不会改变小鼠PVN中小细胞和大细胞神经元的CRF mRNA表达；（iii）急性应激使小鼠和大鼠PVN中的c-fos和CRF mRNA增加到相似程度。因此，在应激和渗透刺激后，小鼠和大鼠下丘脑CRF和CRFR-1基因表达的调节可能存在差异。
