SEXUAL DIMORPHISM AND TESTOSTERONE-DEPENDENT REGULATION OF SOMATOSTATIN GENE-EXPRESSION IN THE PERIVENTRICULAR NUCLEUS OF THE RAT-BRAIN
SEXUAL DIMORPHISM AND TESTOSTERONE-DEPENDENT REGULATION OF SOMATOSTATIN GENE-EXPRESSION IN THE PERIVENTRICULAR NUCLEUS OF THE RAT-BRAIN
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DOI：
10.1210/endo-125-1-357
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发表时间：
1989-07-01
期刊：
影响因子：
4.8
通讯作者：
CLIFTON, DK
中科院分区：
文献类型：
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作者：
CHOWENBREED, JA;STEINER, RA;CLIFTON, DK
下丘脑生长抑素（SS）分泌的性别差异可能部分解释了大鼠GH分泌的性别二态性模式。由于男性有较低的基线血清GH水平比女性，SS抑制GH分泌，我们假设，SS神经元在室周核（PeN）的雄性大鼠将有更大的生物合成活性比女性。我们测试了这一假设，通过测量SS mRNA在细胞中的完整的雄性和发情前期雌性大鼠的Pen。使用原位杂交和计算机图像分析系统，我们测量了SS mRNA的含量在个别细胞中的PeN和比较信号水平（放射自显影颗粒每细胞）之间的男性和发情前期的女性动物。雄性的PeN细胞中SS mRNA的信号水平显著高于发情前期雌性（雄性，210 ± 0.01）。7粒/细胞;雌性，158 . ±. 5粒/细胞; P < 0.0005），而在额叶皮质的SS细胞中没有观察到差异（雄性，100 ± 0.5粒/细胞; 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环境对下丘脑神经元产生影响的结果。为了检验睾酮刺激PeN神经元中SS基因表达的假设，将成年雄性大鼠阉割，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，其尺寸将递送生理水平的睾酮（3.6 ± 1.5）。1.5 ng/ml）。我们观察到，与完整动物相比，去势动物在PeN的神经元中具有显著较低水平的SS mRNA信号（完整，195 . ±. 3粒/细胞;去势，159 . ±. 6粒/细胞; P < 0.003），并且生理水平的睾酮阻止SS mRNA水平的这种降低（去势睾酮替代，182 . ±. 4粒/细胞;去势，159 . ±. 6粒/细胞; P < 0.003）。此外，睾丸酮处理的去势动物的SS mRNA信号水平与完整对照动物的SS mRNA信号水平（完整，195 ± 0.01）没有区别。3粒细胞;去势睾酮替代，182 . ±. 4格令/细胞）。在额叶皮层神经元中SS mRNA水平没有显著差异（完整，98 . ±. 2粒/细胞;去势，98 . ±. 3粒/细胞;去势睾酮替代，102 . ±. 2粒/细胞）。基于这些观察结果，我们推断，男性和女性动物之间的GH分泌谱的差异可能会发生凭借性二型SS基因在下丘脑的表达;此外，观察到的性二型SS mRNA水平可能是部分归因于不同的激素环境之间的性别与睾酮刺激SS基因表达的神经元的PeN。
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 < 0.0005), whereas no differences 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 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 < 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 < 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). Based on these observations we infer that differences in the GH secretory profile between male and female animals may occur by virtue of sexually dimorphic SS gene expression in the hypothalamus; moreover, the observed sexual dimorphism in SS mRNA levels may be attribute in part to the different hormonal environments between the sexes with testosterone stimulating SS gene expression in neurons of the PeN.