Biology Department, Boston University, Boston, Massachusetts, USA.
J Neurophysiol. 2011 Feb;105(2):601-14. doi: 10.1152/jn.00883.2010. Epub 2010 Dec 8.
Reproductive behaviors of many vertebrate species are activated in adult males by elevated androgen levels and abolished by castration. Neural and muscular components controlling these behaviors contain numerous hormone-sensitive sites including motor initiation centers (such as the basal ganglia), central pattern generators (CPGs), and muscles; therefore it is difficult to confirm the role of each hormone-activated target using behavioral assays alone. Our goal was to address this issue by determining the site of androgen-induced vocal activation using male Xenopus laevis, a species in which androgen dependence of vocal activation has been previously determined. We compared in vivo calling patterns and functionality of two in vitro preparations-the isolated larynx and an isolated brain from which fictive courtship vocalizations can be evoked--in castrated and control males. The isolated larynx allowed us to test whether castrated males were capable of transducing male-typical nerve signals into vocalizations and the fictively vocalizing brain preparation allowed us to directly examine vocal CPG function separate from the issue of vocal initiation. The results indicate that all three components--vocal initiation, CPG, and larynx--require intact gonads. Vocal production decreased dramatically in castrates and laryngeal contractile properties of castrated males were demasculinized, whereas no changes were observed in control animals. In addition, fictive calls of castrates were degraded compared with those of controls. To our knowledge, this finding represents the first demonstration of gonad-dependent maintenance of a CPG for courtship behavior in adulthood. Because previous studies showed that androgen-replacement can prevent castration-induced vocal impairments, we conclude that degradation of vocal initiation centers, larynx, and CPG function are most likely due to steroid hormone deprivation.
许多脊椎动物物种的生殖行为在成年雄性中通过升高的雄激素水平激活,并通过阉割而消除。控制这些行为的神经和肌肉成分包含许多激素敏感部位,包括运动起始中心(如基底神经节)、中枢模式发生器(CPGs)和肌肉;因此,仅通过行为测定很难确认每种激素激活的靶位的作用。我们的目标是通过确定使用雄性非洲爪蟾(Xenopus laevis)的雄激素诱导发声的部位来解决这个问题,该物种先前已经确定了雄激素依赖性发声。我们比较了两种体内叫声模式和功能体外制剂-分离的喉和可以诱发虚构求偶叫声的分离脑-在阉割和对照雄性中。分离的喉使我们能够测试阉割雄性是否能够将典型的雄性神经信号转化为发声,而虚构发声的脑制剂使我们能够直接检查发声 CPG 功能,而无需考虑发声起始的问题。结果表明,所有三个组成部分-发声起始,CPG 和喉-都需要完整的性腺。阉割后发声明显减少,阉割雄性的喉收缩特性去雄性化,而对照动物则没有观察到变化。此外,与对照相比,虚构的叫声受损。据我们所知,这一发现代表了在成年期首次证明了求偶行为的 CPG 依赖于性腺维持的发现。由于先前的研究表明雄激素替代可以预防阉割引起的发声障碍,因此我们得出结论,发声起始中心,喉和 CPG 功能的退化很可能是由于类固醇激素剥夺所致。