Matsumoto Akira
Department of Anatomy, Juntendo University School of Medicine, Hongo, Tokyo, Japan.
Stress. 2005 Jun;8(2):133-40. doi: 10.1080/10253890500140642.
Chronic stress is known to induce disorders of reproductive neuroendocrine functions. Motoneurons of the spinal nucleus of the bulbocavernosus (SNB) in male rats play an important role in copulatory behavior. In the present study, it was examined whether chronic stress would alter synaptic organization of the SNB motoneurons and whether androgen would modify the changes under chronic stress. Five male rats were under restraint stress for 5 days per week for 3 weeks, and five males implanted subcutaneously with Silastic capsules containing testosterone were also exposed to stress. Five males served as unstressed controls. After 3 weeks of restraint stress, cholera toxin-horseradish peroxidase (CT-HRP) was injected into the bulbocavernosus muscles and animals were killed 2 days later. The spinal cords containing the SNB were dissected, processed with a modified tetramethylbenzidine (TMB) method for visualization of retrogradely transported CT-HRP, and examined ultrastructurally. Neuronal structures apposing the membranes of 150 SNB motoneurons (total for three groups) were analyzed by measuring the percentage of somatic membranes covered by synaptic contacts. The mean percentage of somatic membranes covered by synapses in males exposed to chronic stress was significantly less than that in controls or stressed males treated with testosterone. Size and number of synaptic contacts per unit length of somatic membranes in males exposed to stress were also significantly less than those in controls or stressed males treated with testosterone. There was no significant difference in any of the parameters between controls and stressed males treated with testosterone. Changes in plasma levels of testosterone showed the same profile as changes in the synaptic contacts. These results suggest that the SNB motoneurons of male rats exposed to chronic stress retain a considerable synaptic plasticity in response to androgen, and that androgen treatment can rescue the SNB system in male rats when under chronic restraint stress.
已知慢性应激会诱发生殖神经内分泌功能紊乱。雄性大鼠球海绵体肌脊髓核(SNB)的运动神经元在交配行为中起重要作用。在本研究中,检测了慢性应激是否会改变SNB运动神经元的突触组织,以及雄激素是否会改变慢性应激下的这些变化。五只雄性大鼠每周接受5天的束缚应激,持续3周,另外五只皮下植入含睾酮的硅橡胶胶囊的雄性大鼠也接受应激处理。五只雄性大鼠作为未应激对照组。束缚应激3周后,将霍乱毒素 - 辣根过氧化物酶(CT - HRP)注入球海绵体肌,2天后处死动物。解剖含有SNB的脊髓,用改良的四甲基联苯胺(TMB)方法处理以可视化逆行转运的CT - HRP,并进行超微结构检查。通过测量被突触接触覆盖的体细胞细胞膜百分比,分析了150个SNB运动神经元(三组总计)膜相邻的神经元结构。暴露于慢性应激的雄性大鼠中,被突触覆盖的体细胞细胞膜的平均百分比显著低于对照组或接受睾酮治疗的应激雄性大鼠。暴露于应激的雄性大鼠中,体细胞细胞膜单位长度上突触接触的大小和数量也显著低于对照组或接受睾酮治疗的应激雄性大鼠。对照组和接受睾酮治疗的应激雄性大鼠在任何参数上均无显著差异。睾酮血浆水平的变化与突触接触的变化呈现相同的趋势。这些结果表明,暴露于慢性应激的雄性大鼠的SNB运动神经元在对雄激素的反应中保留了相当大的突触可塑性,并且雄激素治疗可以在慢性束缚应激下挽救雄性大鼠的SNB系统。