Meister B, Broberger C, Villar M J, Hökfelt T
Department of Neuroscience, Berzelius Laboratory, Karolinska Institute, Stockholm, Sweden.
Neuroendocrinology. 1994 Nov;60(5):458-69. doi: 10.1159/000126782.
Magnocellular neurons of the supraoptic (SON) and paraventricular (PVN) nuclei projecting to the neurohypophysis produce, in addition to the classical hormones vasopressin and oxytocin, a large number of other peptides, one of which is cholecystokinin (CCK). Binding sites for CCK have been identified in the posterior pituitary. Recently the cDNAs for CCKA and CCKB receptors were isolated and characterized, and CCKA and CCKB receptor mRNAs were localized in the SON and PVN. We have used complementary oligonucleotides and in situ hybridization histochemistry to study CCKB receptor mRNA in hypothalamic neurons. Changes in the expression of CCKB receptor mRNA in the SON and PVN were analysed in salt-loaded as well as in hypophysectomized animals. Levels of CCKB receptor mRNA in the PVN and SON increased markedly in salt-loaded animals as compared to controls. An increase in CCKB receptor mRNA levels was seen in the SON and PVN after 3 days of salt loading, with high levels continuing through 5 and 7 days. At 14 days, the levels of CCKB receptor mRNA in the PVN were significantly lower as compared to 7 days. Hypophysectomy 5 days prior to sacrifice, resulting in a nerve lesion in the neurohypophysial pathway and removal of the anterior pituitary hormones, induced a significant increase in CCKB receptor mRNA levels in neurons of the PVN. The increase in CCKB receptor mRNA labelling after salt loading was mainly observed in the ventrolateral part of the PVN and in the dorsolateral part of the SON, corresponding to oxytocin-containing neurons, whereas the increase after hypophysectomy was mainly seen in the central part of the PVN and in the ventral part of the SON, corresponding to vasopressin-containing neurons. The results suggest that the synthesis of CCKB receptors in magnocellular neurons is increased upon osmotic challenge and hypophysectomy.
投射至神经垂体的视上核（SON）和室旁核（PVN）的大细胞神经元，除了产生经典激素血管加压素和催产素外，还能产生大量其他肽类，其中之一是胆囊收缩素（CCK）。已在垂体后叶中鉴定出CCK的结合位点。最近，CCKA和CCKB受体的cDNA被分离并进行了表征，且CCKA和CCKB受体mRNA定位于SON和PVN。我们使用互补寡核苷酸和原位杂交组织化学方法研究下丘脑神经元中的CCKB受体mRNA。分析了盐负荷动物以及垂体切除动物中SON和PVN中CCKB受体mRNA表达的变化。与对照组相比，盐负荷动物PVN和SON中CCKB受体mRNA水平显著升高。盐负荷3天后SON和PVN中CCKB受体mRNA水平升高，高水平持续至5天和7天。在14天时，PVN中CCKB受体mRNA水平与7天时相比显著降低。处死前5天进行垂体切除，导致神经垂体通路神经损伤并去除垂体前叶激素，可诱导PVN神经元中CCKB受体mRNA水平显著升高。盐负荷后CCKB受体mRNA标记的增加主要见于PVN的腹外侧部分和SON的背外侧部分，对应含催产素的神经元，而垂体切除后增加主要见于PVN的中央部分和SON的腹侧部分，对应含血管加压素的神经元。结果表明，在渗透刺激和垂体切除时，大细胞神经元中CCKB受体的合成增加。
