Chowen-Breed J A, Steiner R A, Clifton D K
Department of Physiology and Biophysics, University of Washington, Seattle 98195.
Endocrinology. 1989 Jul;125(1):357-62. doi: 10.1210/endo-125-1-357.
Gender differences in hypothalamic somatostatin (SS) secretion may account in part for the sexually dimorphic patterns of GH secretion in rats. Since males have lower baseline serum GH levels than females, and SS inhibits GH secretion, we hypothesized that the SS neurons in the periventricular nucleus (PeN) of the male rat would have greater biosynthetic activity than those of the female. We tested this hypothesis by measuring SS mRNA in cells in the PeN of intact male and proestrous female rats. Using in situ hybridization and a computerized image analysis system, we measured SS mRNA content in individual cells in the PeN and compared signal levels (autoradiographic grains per cell) between male and proestrous female animals. The signal level of SS mRNA in cells of the PeN was significantly greater in males than in proestrous females (males, 210 +/- 7 grains/cell; females, 158 +/- 5 grains/cell; P less than 0.0005), whereas no difference was observed in SS cells of the frontal cortex (males, 100 +/- 0.8 grains/cell; females, 99 +/- 5.9 grains/cell). This difference in SS mRNA levels is likely to be the result of different hormonal environments exerting an influence on neurons of the hypothalamus. To test the hypothesis that testosterone stimulates SS gene expression in neurons of the PeN, adult male rats were castrated and immediately implanted with either empty (sham; n = 3) or testosterone-containing (n = 3) Silastic implants of a size that would deliver physiological levels of testosterone (3.6 +/- 1.5 ng/ml). We observed that castrated animals had significantly lower levels of SS mRNA signal in neurons of the PeN compared with intact animals (intact, 195 +/- 3 grains/cell; castrated, 159 +/- 6 grains/cell; P less than 0.003) and that physiological levels of testosterone prevent this reduction in SS mRNA levels (castrated testosterone-replaced, 182 +/- 4 grains/cell; castrated, 159 +/- 6 grains/cell; P less than 0.003). Furthermore, testosterone-treated castrates had SS mRNA signal levels indistinguishable from those of intact controls (intact, 195 +/- 3 grains/cell; castrated testosterone-replaced, 182 +/- 4 grains/cell). There was no significant difference in SS mRNA levels in neurons of the frontal cortex (intact, 98 +/- 2 grains/cell; castrated, 98 +/- 3 grains/cell; castrated testosterone-replaced, 102 +/- 2 grains/cell).(ABSTRACT TRUNCATED AT 400 WORDS)
下丘脑生长抑素（SS）分泌的性别差异可能部分解释了大鼠生长激素（GH）分泌的性别二态性模式。由于雄性大鼠的基础血清GH水平低于雌性，且SS抑制GH分泌，我们推测雄性大鼠室周核（PeN）中的SS神经元比雌性具有更高的生物合成活性。我们通过测量完整雄性和动情前期雌性大鼠PeN中细胞的SS mRNA来验证这一假设。使用原位杂交和计算机图像分析系统，我们测量了PeN中单个细胞的SS mRNA含量，并比较了雄性和动情前期雌性动物之间的信号水平（每个细胞的放射自显影片颗粒数）。PeN细胞中SS mRNA的信号水平在雄性中显著高于动情前期雌性（雄性，210±7颗粒/细胞；雌性，158±5颗粒/细胞；P<0.0005），而在额叶皮质的SS细胞中未观察到差异（雄性，100±0.8颗粒/细胞；雌性，99±5.9颗粒/细胞）。SS mRNA水平的这种差异可能是不同激素环境对下丘脑神经元产生影响的结果。为了验证睾酮刺激PeN神经元中SS基因表达的假设，对成年雄性大鼠进行阉割，并立即植入空的（假手术；n = 3）或含睾酮的（n = 3）硅橡胶植入物，其大小可提供生理水平的睾酮（3.6±1.5 ng/ml）。我们观察到，与完整动物相比，阉割动物PeN神经元中的SS mRNA信号水平显著降低（完整动物，195±3颗粒/细胞；阉割动物，159±6颗粒/细胞；P<0.003），且生理水平的睾酮可防止SS mRNA水平的这种降低（阉割后补充睾酮，182±4颗粒/细胞；阉割动物，159±6颗粒/细胞；P<0.003）。此外，经睾酮处理的阉割动物的SS mRNA信号水平与完整对照无显著差异（完整动物，195±3颗粒/细胞；阉割后补充睾酮，182±4颗粒/细胞）。额叶皮质神经元中的SS mRNA水平无显著差异（完整动物，98±2颗粒/细胞；阉割动物，98±3颗粒/细胞；阉割后补充睾酮，102±2颗粒/细胞）。（摘要截短至400字）
