Department of Anatomy and Neurobiology, University of Kentucky College of Medicine, 800 Rose Street, Lexington, Kentucky 40536-0084; and Department of Physiology, Southern Illinois University School of Medicine, Carbondale, Illinois 62901.
Mol Cell Neurosci. 1993 Jun;4(3):298-303. doi: 10.1006/mcne.1993.1038.
The peptide galanin is localized in lactotrophs, somatotrophs, and thyrotrophs of the female rat anterior pituitary gland (AP). These cell types are absent in the AP of the Ames dwarf mouse. Moreover, estrogen increases galanin gene expression in the rat AP, but has little effect on galanin in the hypothalamus. The objectives of this study were to (i) determine whether estrogen increases galanin gene expression in the normal mouse AP or hypothalamus, and (ii) compare the distribution of galanin peptide in the hypothalamopituitary axis of normal and Ames dwarf mice. Adult female mice (normal and Ames dwarf) were treated with estrogen pellets (0.25 mg; sc) for 2 weeks. Estrogen increased galanin peptide levels fivefold in the normal mouse AP, but did not alter peptide levels in the neurointermediate lobe or hypothalamus. Galanin peptide levels were undetectable in the AP of the dwarf mouse. In addition, galanin peptide levels in the hypothalamus of the dwarf mice were 30% lower than in normal mice, regardless of the steroid treatment. Galanin peptide levels in the neurointermediate lobe were similar in dwarf and control mice. Galanin mRNA levels were undetectable in the AP of estrogen-treated dwarf mice by Northern blot analysis and were elevated by estrogen in the AP of normal mice. Galanin mRNA levels were similar in the hypothalamus of normal and dwarf mice and were unchanged by estrogen. The following conclusions were drawn: (i) Estrogen increases galanin gene expression in the normal mouse AP but has no effect in the hypothalamus; (ii) galanin peptide is undetectable in the AP of Ames dwarf mice, lower in the hypothalamus, and unchanged in the neurointermediate lobe compared to normal mice; and (iii) galanin mRNA is present in similar quantities in normal and Ames dwarf mouse hypothalamus, whereas galanin mRNA is undetectable in the dwarf mouse AP.
肽类胆囊收缩素定位于雌性大鼠前垂体腺(AP)的乳突细胞、生长激素细胞和促甲状腺激素细胞。这些细胞类型不存在于 Ames 侏儒鼠的 AP 中。此外,雌激素增加了大鼠 AP 中的胆囊收缩素基因表达,但对下丘脑的胆囊收缩素影响不大。本研究的目的是:(i)确定雌激素是否增加正常小鼠 AP 或下丘脑的胆囊收缩素基因表达,以及(ii)比较正常和 Ames 侏儒小鼠下丘脑-垂体轴中胆囊收缩素肽的分布。成年雌性小鼠(正常和 Ames 侏儒)接受雌激素丸(0.25mg;sc)治疗 2 周。雌激素使正常小鼠 AP 中的胆囊收缩素肽水平增加了五倍,但没有改变神经中间叶或下丘脑的肽水平。侏儒鼠的 AP 中检测不到胆囊收缩素肽。此外,无论接受类固醇治疗与否,侏儒鼠下丘脑的胆囊收缩素肽水平比正常小鼠低 30%。侏儒鼠和对照组的神经中间叶的胆囊收缩素肽水平相似。Northern 印迹分析显示,雌激素处理的侏儒鼠 AP 中无法检测到胆囊收缩素 mRNA,而正常鼠 AP 中的胆囊收缩素 mRNA 则被雌激素上调。正常和侏儒鼠的下丘脑的胆囊收缩素 mRNA 水平相似,且不受雌激素影响。得出以下结论:(i)雌激素增加了正常小鼠 AP 中的胆囊收缩素基因表达,但对下丘脑没有影响;(ii)Ames 侏儒鼠的 AP 中无法检测到胆囊收缩素肽,其在下丘脑中的含量较低,而在神经中间叶中与正常小鼠相比没有变化;(iii)与正常的 Ames 侏儒鼠相比,正常和 Ames 侏儒鼠的下丘脑胆囊收缩素 mRNA 水平相似,而侏儒鼠的 AP 中则检测不到胆囊收缩素 mRNA。