Author(s): Yoshiki Matsumoto, Takanori Miki, Katsuhiko Warita, Zhi-Yu Wang, Tomiko Yakura, Jun-Qian Liu and Yoshiki Takeuchi
In transgenic Mini rat, in which the expression of intrinsic growth hormone (GH) gene is suppressed by the antisense GH transgene are characterized by definite somatic growth retardation at puberty. Compared to age-matched wild-type Wister (non-Mini) rat, Mini rat showed low blood GH levels and GH cell depletion in the anterior pituitary (AP). The AP and periventricular hypothalamic nucleus (PeVN) were processed for immunohistochemical analysis with antisera to Luteinizing hormone (LH) and somatostatin (SOM), respectively. Although LH-immunoreactive (IR) cells showed the decrease in number in Mini rat from 4 to 8 weeks of age, there was the significant increase in non-Mini rat. Interestingly, SOM-IR cells in the PeVN showed the marked increase in number in Mini rat in contrast to the decrease in non-Mini rat during the same periods. The testis weights were not significantly different between Mini and non-Mini rat at 4 weeks of age, whereas at 6 and 8 weeks of age the value of Mini rat was significantly smaller than non-Mini rat. It was concluded that the onset and development of LH-testicular axis need intrinsic GH regulation, which is involved the SOM cell interaction from PeVN, and the SOM plays a crucial role in the development of pituitary-testicular maturation during the puberty.