Lubischer J L, Arnold A P
Program in Neuroscience, University of California, Los Angeles 90095-1761, USA.
Brain Res. 1995 Oct 2;694(1-2):61-8. doi: 10.1016/0006-8993(95)00766-j.
Testosterone is an important trophic factor for motoneurons in the spinal nucleus of the bulbocavernosus (SNB), and SNB motoneurons are more responsive to testosterone than are other motoneurons. Axonal injury during early postnatal life prevents the normal development of steroid-sensitivity by adult SNB motoneurons. Axonal injury also causes changes in the expression by motoneurons of a wide range of proteins, including the up-regulation of trophic factor receptors. We have used a polyclonal antibody (PG-21; G.S. Prins) to study the expression of androgen receptors in SNB motoneurons after axonal injury. PG-21 labeled motoneuronal nuclei in the lower lumbar spinal cord of rats in a pattern that matched autoradiographic reports of androgen accumulation in this region of the nervous system. A population of numerous, small cells located dorsal to the central canal also showed evidence of androgen receptor expression. Cutting the axons of SNB motoneurons in adulthood or in development caused a decrease in androgen receptor immunoreactivity in SNB motoneurons. This is the first report that a trophic factor receptor in motoneurons is down-regulated after axonal injury, and is interesting in light of reports that testosterone treatment can facilitate motoneuronal regeneration after nerve cut. Androgen receptor levels subsequently returned to normal, regardless of the age at axotomy, providing no evidence for a lasting effect of developmental axotomy on androgen receptor levels in SNB motoneurons. Thus, axotomy-induced down-regulation of androgen receptors does not underlie the inability of SNB motoneurons to respond to androgen treatment several months after pudendal nerve cut in development.
睾酮是球海绵体肌脊髓核（SNB）中运动神经元的重要营养因子，且SNB运动神经元比其他运动神经元对睾酮更敏感。出生后早期的轴突损伤会阻碍成年SNB运动神经元类固醇敏感性的正常发育。轴突损伤还会导致运动神经元中多种蛋白质的表达发生变化，包括营养因子受体的上调。我们使用一种多克隆抗体（PG - 21；G.S. Prins）来研究轴突损伤后SNB运动神经元中雄激素受体的表达。PG - 21标记大鼠下腰脊髓中的运动神经元细胞核，其模式与该神经系统区域雄激素积累的放射自显影报告相符。位于中央管背侧的大量小细胞群体也显示出雄激素受体表达的证据。在成年期或发育期切断SNB运动神经元的轴突会导致SNB运动神经元中雄激素受体免疫反应性降低。这是首次报道运动神经元中的一种营养因子受体在轴突损伤后下调，鉴于有报道称睾酮治疗可促进神经切断后运动神经元的再生，这一发现很有趣。无论轴突切断时的年龄如何，雄激素受体水平随后都会恢复正常，这表明发育期轴突切断对SNB运动神经元中雄激素受体水平没有持久影响。因此，轴突切断诱导的雄激素受体下调并不是SNB运动神经元在发育期阴部神经切断数月后无法对雄激素治疗产生反应的原因。
