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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Gonadal hormones affect spine synaptic density in the CA1 hippocampal subfield of male rats.
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Gonadal hormones affect spine synaptic density in the CA1 hippocampal subfield of male rats.

机译:性腺激素影响雄性大鼠CA1海马亚区的脊柱突触密度。

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The effects of androgen on the density of spine synapses on pyramidal neurons in the CA1 area of the hippocampus were studied in male rats. Gonadectomy (GDNX) had no significant effect on the number of CA1 pyramidal cells but reduced CA1 spine synapse density by almost 50% (to 0.468 +/- 0.018 spine synapses/microm(3)) compared with sham-operated controls (0.917 +/- 0.06 spine synapses/microm(3)). Treatment of GDNX rats with testosterone propionate (500 microg/d, s.c., 2 d) increased spine synapse density to levels (1.01 +/- 0.026 spine synapses/microm(3)) comparable with intact males. A similar increase in synapse density (1.013 +/- 0.05 spine synapses/microm(3)) was observed in GDNX animals after treatment with dihydrotestosterone (DHT) (500 microg/d, s.c., 2 d) but not after estradiol (10 microg/d, s.c., 2 d; 0.455 +/- 0.02 spine synapse/microm(3)). These data indicate that testosterone is important for maintenance of normal spine synapse density in the CA1 region of the male rat hippocampus. The comparable responses to testosterone and the non-aromatizable androgen DHT, coupled with the lack of response to estradiol, suggest that testosterone acts directly on hippocampal androgen receptors rather than indirectly via local estrogen biosynthesis.
机译:在雄性大鼠中研究了雄激素对海马CA1区锥体神经元脊柱突触密度的影响。与假手术对照组(0.917 + /)相比,性腺切除术(GDNX)对CA1锥体细胞的数量没有显着影响,但将CA1脊柱突触密度降低了近50%(至0.468 +/- 0.018脊柱突触/微米(3))。 -0.06脊柱突触/微米(3))。用丙酸睾丸酮(500 microg / d,s.c.,2 d)治疗GDNX大鼠使脊柱突触密度增加至与完整雄性可比的水平(1.01 +/- 0.026脊柱突触/ microm(3))。在用二氢睾酮(DHT)(500 microg / d,sc,2 d)治疗后,在GDNX动物中观察到类似的突触密度增加(1.013 +/- 0.05脊柱突触/微米(3)),但在雌二醇(10 microg / d,sc,2天; 0.455 +/- 0.02脊柱突触/微米(3))。这些数据表明睾丸激素对于维持雄性大鼠海马CA1区正常脊柱突触密度很重要。对睾丸激素和不可芳香化雄激素DHT的可比反应,再加上对雌二醇的反应不足,表明睾丸激素直接作用于海马雄激素受体,而不是通过局部雌激素的生物合成间接作用。

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