Eagleson G W, Malacinski G M
Anat Rec. 1986 Jul;215(3):317-27. doi: 10.1002/ar.1092150314.
A scanning electron microscopy, histological, and immunochemical investigation examined the effects of the mutant gene (e) upon hypothalamic development in the Mexican axolotl. The adult eyeless mutant is sterile. Previous studies indicated that this reproductive defect was due to the mutation's effect upon the hypothalamus. The present study demonstrated the pleiotropic effects of the eyeless gene upon development of the hypothalamus. Scanning electron microscopy studies looked at the early ontogeny of the hypothalamohypophyseal system. The major morphological difference observed in the hypothalamus of normals compared to eyeless mutants was the reduced nature or complete lack of a preoptic recess in eyeless mutants. Early embryonic tissue movements also differed when normal siblings were compared to eyeless mutant axolotls. Histological examination looking for paraldehyde-fuchsin-positive secretory neurons revealed a paired nucleus preopticus in both normals and eyeless mutants, but this region lacked the emanating paraldehyde-fuchsin-positive fiber tracts in eyeless mutants. The neurohypophysis of the eyeless mutants was atrophied and contained far less paraldehyde-fuchsin-positive material when compared to normal axolotls. Immunochemical studies were done to look at the distribution of immunoreactive luteinizing-hormone-releasing hormone (ir-LHRH) in brains of eyed and eyeless mutant axolotls of different stages. This study detected deficiencies in ir-LHRH in the anterior hypothalamus of eyeless mutants. In general in the eyeless mutant axolotl, the observed anterior hypothalamic deficiencies are comparable to those observed in anurans which have had their optic vesicles removed. These observations suggest a possible utility of the eyeless mutant axolotl for studies concerned with endocrine development in the absence of hypothalamic modulation.
一项扫描电子显微镜、组织学和免疫化学研究，考察了突变基因（e）对墨西哥钝口螈下丘脑发育的影响。成年无眼突变体是不育的。先前的研究表明，这种生殖缺陷是由于该突变对下丘脑的影响所致。本研究证明了无眼基因对下丘脑发育具有多效性作用。扫描电子显微镜研究观察了下丘脑 - 垂体系统的早期个体发育。与无眼突变体相比，正常个体下丘脑观察到的主要形态学差异是，无眼突变体中视前隐窝的性质减弱或完全缺失。与无眼突变体钝口螈相比，正常同胞的早期胚胎组织运动也有所不同。寻找副醛 - 品红阳性分泌神经元的组织学检查显示，正常个体和无眼突变体中均有视前成对核，但在无眼突变体中，该区域缺乏发出的副醛 - 品红阳性纤维束。与正常钝口螈相比，无眼突变体的神经垂体萎缩，且含有的副醛 - 品红阳性物质少得多。进行了免疫化学研究，以观察不同阶段有眼和无眼突变体钝口螈大脑中免疫反应性促黄体生成激素释放激素（ir - LHRH）的分布。本研究检测到无眼突变体下丘脑前部的ir - LHRH存在缺陷。一般来说，在无眼突变体钝口螈中，观察到的下丘脑前部缺陷与那些切除了视泡的无尾两栖类动物中观察到的缺陷相当。这些观察结果表明，无眼突变体钝口螈对于研究在没有下丘脑调节情况下的内分泌发育可能具有一定用途。
