Yashiro T, Arai M, Miyashita E, Yamashita K, Suzuki T
Department of Anatomy, St. Marianna University School of Medicine, Kawasaki, Japan.
Cell Tissue Res. 1988 Feb;251(2):249-55. doi: 10.1007/BF00215832.
Snell dwarf mice display remarkable retardation of growth after birth and are known to lack prolactin (PRL), thyroid stimulating hormone (TSH) and growth hormone (GH). The aim of this study was to determine the reason for these hormonal deficiencies. We examined the fine structure of the gland and its immunohistochemical staining pattern with respect to antisera raised against PRL, TSH, GH, adrenocorticotrophic hormone (ACTH) and luteinizing hormone (LH). The gland of control mice reacted immunohistochemically against all antisera used, whereas only ACTH-producing cells (ACTH cells) and LH-producing cells (LH cells) were distinguished in the dwarf mice. ACTH cells in dwarf mice varied in cell shape, although they were similar in size to those of controls. The distribution of secretory granules in the cytoplasm varied from cell to cell. LH cells in the dwarf mice showed immature features, having poorly developed rough endoplasmic reticulum and Golgi apparatus. The cells were about half the size of controls, and secretory granules were smaller. In dwarf mice, non-granulated cells were encountered in addition to granulated ACTH and LH cells. Some of them formed small clusters, characteristic cell junctions being found between the cells; they thus appeared to be follicular cells. The above results suggest that hormone deficiency in Snell dwarf mice is a result of a defect in the hormone-producing cells in the gland.
斯内尔侏儒小鼠出生后生长显著迟缓，已知其缺乏催乳素（PRL）、促甲状腺激素（TSH）和生长激素（GH）。本研究的目的是确定这些激素缺乏的原因。我们针对抗PRL、TSH、GH、促肾上腺皮质激素（ACTH）和黄体生成素（LH）的抗血清，检查了该腺体的精细结构及其免疫组织化学染色模式。对照小鼠的腺体对所有使用的抗血清均产生免疫反应，而在侏儒小鼠中仅区分出促肾上腺皮质激素分泌细胞（ACTH细胞）和黄体生成素分泌细胞（LH细胞）。侏儒小鼠的ACTH细胞形状各异，尽管其大小与对照小鼠的相似。细胞质中分泌颗粒的分布因细胞而异。侏儒小鼠的LH细胞呈现不成熟的特征，粗面内质网和高尔基体发育不良。这些细胞大小约为对照小鼠细胞的一半，分泌颗粒也较小。在侏儒小鼠中，除了颗粒状的ACTH和LH细胞外，还发现了无颗粒细胞。其中一些形成小簇，细胞之间存在特征性的细胞连接；因此它们似乎是滤泡细胞。上述结果表明，斯内尔侏儒小鼠的激素缺乏是该腺体中激素产生细胞缺陷的结果。
