Burke K A, Widows M R, Sengelaub D R
Program in Neural Science, Indiana University, Bloomington 47405, USA.
J Neurobiol. 1997 Jul;33(1):1-10. doi: 10.1002/(sici)1097-4695(199707)33:1<1::aid-neu1>3.0.co;2-7.
The rat lumbar spinal cord contains the testosterone-dependent spinal nucleus of the bulbocavernosus (SNB), whose motoneurons innervate perineal muscles involved in copulatory reflexes. In normal males, SNB dendrites grow exuberantly through the first 4 weeks postnatally. This growth is steroid-dependent: dendrites fail to grow in males castrated at P7, but grow normally in castrates treated with testosterone (T). Treatment with either of the T metabolites, dihydrotestosterone or estrogen, supports dendritic growth in castrates, but not to the lengths characteristic of intact males or T-treated castrates. The present study tested the hypothesis that dihydrotestosterone and estrogen act together to support development of SNB dendrites. Male rat pups were castrated on P7 and treated daily with dihydrotestosterone propionate (DHT) (2 mg), estradiol benzoate (E) (100 microg), DHT (2 mg) combined with estradiol benzoate in either 5 microg (E5) or 100 microg (E100) doses, or vehicle alone. On P28, when SNB dendritic length is normally maximal, motoneurons were retrogradely labeled with cholera toxin-HRP (BHRP). Soma size and dendritic lengths of labeled motoneurons were assessed and compared to those of age-matched, intact male rats. Soma areas of DHT + E5-treated and DHT + E100-treated castrates did not differ from those of castrates treated with DHT alone, although somata of all three groups were significantly larger than those of normal males and E- or oil-treated castrates. Dendritic lengths in DHT + E5-treated castrates were significantly shorter than those of normal males, and did not differ from those of castrates receiving DHT or E alone, although all hormone-treated groups had dendritic lengths that were significantly longer than untreated castrates. However, treatment of castrates with DHT + E100 fully supported dendritic growth to levels characteristic of normal males. These results suggest that somal and dendritic growth may occur through separate developmental mechanisms, and that E and DHT act synergistically to support normal masculine SNB dendritic development.
大鼠腰段脊髓包含球海绵体肌的睾酮依赖性脊髓核（SNB），其运动神经元支配参与交配反射的会阴肌。在正常雄性大鼠中，SNB树突在出生后的前4周内旺盛生长。这种生长依赖于类固醇：在出生后第7天阉割的雄性大鼠中，树突无法生长，但在用睾酮（T）治疗的去势大鼠中树突正常生长。用T的两种代谢产物之一，双氢睾酮或雌激素进行治疗，可支持去势大鼠的树突生长，但达不到完整雄性大鼠或T治疗的去势大鼠的特征长度。本研究检验了双氢睾酮和雌激素共同作用以支持SNB树突发育的假说。雄性幼鼠在出生后第7天被阉割，并每天用丙酸双氢睾酮（DHT）（2毫克）、苯甲酸雌二醇（E）（100微克）、DHT（2毫克）与5微克（E5）或100微克（E100）剂量的苯甲酸雌二醇联合治疗，或仅用赋形剂治疗。在出生后第28天，当SNB树突长度通常达到最大值时，用霍乱毒素-HRP（BHRP）对运动神经元进行逆行标记。评估标记运动神经元的胞体大小和树突长度，并与年龄匹配的完整雄性大鼠进行比较。DHT + E5治疗组和DHT + E100治疗组去势大鼠的胞体面积与单独用DHT治疗的去势大鼠无差异，尽管所有三组的胞体均显著大于正常雄性大鼠以及接受E或油治疗的去势大鼠。DHT + E5治疗组去势大鼠的树突长度显著短于正常雄性大鼠，且与单独接受DHT或E治疗的去势大鼠无差异，尽管所有激素治疗组的树突长度均显著长于未治疗的去势大鼠。然而，用DHT + E100治疗去势大鼠可完全支持树突生长至正常雄性大鼠的特征水平。这些结果表明，胞体和树突的生长可能通过不同的发育机制发生，并且E和DHT协同作用以支持正常的雄性SNB树突发育。
