Sohmer H, Freeman S
Department of Physiology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Audiol Neurootol. 1996 May-Jun;1(3):137-47. doi: 10.1159/000259194.
It seems that many auditory maturational events are regulated by thyroid hormone since elevation in thyroid hormone level always precedes the onset of hearing in the fetus-neonate; low thyroid activity in the developing human fetus or rat neonate leads to hearing loss; earlier, elevated thyroid levels in rat neonate lead to earlier onset of hearing. The hormone, bound to its receptors in the nucleus, acts as a transcription factor activating genes which lead to the synthesis of several proteins and enzymes involved in the structural and functional development of many tissues (e.g. brain, heart, kidney, skeletal muscle) including the ear. Several types of congenital hearing loss of unexplained etiology may be due to abnormalities in one or more stages of this gene cascade since several types of congenital hearing loss have been shown to involve defects in genes related to these events.
似乎许多听觉成熟事件都受甲状腺激素调节,因为甲状腺激素水平升高总是先于胎儿-新生儿听力的开始;发育中的人类胎儿或大鼠新生儿甲状腺活动低下会导致听力丧失;早些时候,大鼠新生儿甲状腺水平升高会导致听力开始时间提前。该激素与细胞核中的受体结合,作为一种转录因子激活基因,这些基因导致合成多种参与包括耳朵在内的许多组织(如大脑、心脏、肾脏、骨骼肌)结构和功能发育的蛋白质和酶。几种病因不明的先天性听力损失可能是由于这一基因级联反应中一个或多个阶段的异常,因为已表明几种先天性听力损失涉及与这些事件相关的基因缺陷。