Yang L Y, Verhovshek T, Sengelaub D R
Department of Physiology, Taipei Medical University, Taipei 110, Taiwan.
Endocrinology. 2004 Jan;145(1):161-8. doi: 10.1210/en.2003-0853. Epub 2003 Sep 25.
Testosterone regulates androgen receptor expression, soma size, and dendritic length in motoneurons of the spinal nucleus of the bulbocavernosus (SNB) in adult male rats. Brain-derived neurotrophic factor (BDNF) is also expressed in SNB motoneurons; BDNF maintains SNB soma size in castrates, and interacts with testosterone to regulate androgen receptor expression in SNB motoneurons. This study tested the hypotheses that BDNF promotes SNB dendritic lengths and that BDNF and testosterone interact to maintain dendritic morphology in SNB motoneurons. Adult male rats were castrated; and, 5 wk later, SNB motoneurons were axotomized bilaterally, and BDNF or PBS was applied via cups sutured to the cut axons. After axotomy plus BDNF or PBS application, castrates received implants of testosterone or blank capsules and were killed 24 d later. Additional males of similar age that received sham castration, sham axotomy, and a blank implant served as sham controls. Two days before death, SNB motoneurons were retrogradely labeled with cholera toxin-horseradish peroxidase, and SNB dendritic morphology was reconstructed in three dimensions. Dendritic lengths in blank-implanted castrates treated with PBS were significantly shorter than those of sham controls; treatment with either testosterone or BDNF alone failed to support dendritic length or distribution. However, treatment with both testosterone and BDNF restored dendritic morphology to the level of sham controls. Our findings demonstrate that BDNF interacts with testosterone in the maintenance of SNB dendritic arbors and support the hypothesis that dendritic morphology is regulated by trophic substances that originate in the neuromuscular periphery.
睾酮可调节成年雄性大鼠球海绵体肌脊髓核（SNB）运动神经元中的雄激素受体表达、胞体大小和树突长度。脑源性神经营养因子（BDNF）也在SNB运动神经元中表达；BDNF可维持去势大鼠的SNB胞体大小，并与睾酮相互作用以调节SNB运动神经元中的雄激素受体表达。本研究检验了以下假设：BDNF可促进SNB树突长度的增长，且BDNF与睾酮相互作用以维持SNB运动神经元的树突形态。对成年雄性大鼠进行去势手术；5周后，双侧切断SNB运动神经元的轴突，并通过缝合在切断轴突上的套管施加BDNF或磷酸盐缓冲液（PBS）。在轴突切断并施加BDNF或PBS后，去势大鼠接受睾酮植入物或空白胶囊植入，并在24天后处死。接受假去势、假轴突切断和空白植入物的同龄雄性大鼠作为假手术对照。处死前2天，用霍乱毒素-辣根过氧化物酶对SNB运动神经元进行逆行标记，并对SNB树突形态进行三维重建。用PBS处理的植入空白胶囊的去势大鼠的树突长度明显短于假手术对照；单独使用睾酮或BDNF均无法维持树突长度或分布。然而，同时使用睾酮和BDNF可使树突形态恢复到假手术对照的水平。我们的研究结果表明，BDNF与睾酮相互作用以维持SNB树突分支，并支持树突形态受源自神经肌肉外周的营养物质调节这一假设。
