Department of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853, USA.
Horm Behav. 2012 Sep;62(4):426-32. doi: 10.1016/j.yhbeh.2012.07.010. Epub 2012 Aug 4.
Behavioral and neuroendocrine mechanisms of social vocalization in teleost fish are influenced by the glucocorticoid cortisol and the androgen 11-ketotestosterone (11kT). The relative abundance of both 11kT, which binds to androgen receptors (ARα, ARβ), and cortisol, which binds to glucocorticoid receptors (GR-1, GR-2), is regulated by 11β-hydroxylase (11βH) that converts 11-deoxycortisol to cortisol and testosterone to 11β-OH-testosterone, and 11β-hydroxysteroid dehydrogenase (11βHSD) that converts cortisol to the inactive metabolite cortisone and 11β-OH-testosterone to 11kT. In midshipman fish, we tested the hypothesis that plasma steroid levels, mRNA abundance for 11βH and 11βHSD in the vocal muscle and testis (known site of 11kT synthesis), and mRNA abundances for ARs and GRs in vocal muscle, would differ between males that did or did not recently produce 'hum' advertisement calls. Quantitative real-time PCR demonstrated that non-calling male vocal muscle had significantly higher mRNA levels for all receptors except ARα, and a strong trend for higher 11βHSD; 11βH was similar to that in calling males. Calling males had higher plasma and testis 11kT, but lower plasma cortisol, levels. Testis enzyme levels did not differ between male groups, although calling males showed a positive linear correlation between plasma 11kT and testis 11βHSD mRNA levels, consistent with testis being the main source of plasma 11kT. We propose that higher vocal muscle 11βHSD levels in non-calling males reflect increased local conversion of elevated cortisol to cortisone, providing protection from cortisol-related toxicity, while increased receptor expression in non-calling males functions as a preparatory mechanism for meeting the physiological demands of future vocalization.
硬骨鱼类社会发声的行为和神经内分泌机制受糖皮质激素皮质醇和雄激素 11-酮睾酮(11kT)的影响。11β-羟化酶(11βH)将 11-脱氧皮质醇转化为皮质醇和睾酮转化为 11β-OH-睾酮,11β-羟化类固醇脱氢酶(11βHSD)将皮质醇转化为无活性代谢物考的松和 11β-OH-睾酮转化为 11kT,从而调节两者的相对丰度,即结合雄激素受体(ARα、ARβ)的 11kT 和结合糖皮质激素受体(GR-1、GR-2)的皮质醇。在中期雄鱼中,我们验证了以下假设,即血浆类固醇水平、发声肌和睾丸(已知的 11kT 合成部位)中 11βH 和 11βHSD 的 mRNA 丰度,以及发声肌中 AR 和 GR 的 mRNA 丰度,在最近是否产生“嗡嗡”广告叫声的雄性之间会有所不同。定量实时 PCR 表明,非发声雄性发声肌的所有受体(除 ARα 外)的 mRNA 水平均显著升高,11βHSD 水平也呈上升趋势;11βH 与发声雄性相似。发声雄性的血浆和睾丸 11kT 水平较高,但血浆皮质醇水平较低。雄性群体之间的睾丸酶水平没有差异,尽管发声雄性的血浆 11kT 与睾丸 11βHSD mRNA 水平呈正线性相关,这与睾丸是血浆 11kT 的主要来源一致。我们提出,非发声雄性发声肌中较高的 11βHSD 水平反映了皮质醇升高向考的松的局部转化增加,从而提供了对皮质醇相关毒性的保护,而非发声雄性中受体表达的增加则作为未来发声的生理需求的预备机制。