Brain-derived neurotrophic factor and androgen interact in the maintenance of dendritic morphology in a sexually dimorphic rat spinal nucleus

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.