SEX-HORMONES REGULATE ABR LATENCY
SEX-HORMONES REGULATE ABR LATENCY
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DOI：
10.1016/s0194-5998(94)70791-x
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发表时间：
1994-01-01
影响因子：
3.4
通讯作者：
JERGER, JJ
中科院分区：
文献类型：
--
作者：
ELKINDHIRSCH, KE;WALLACE, E;JERGER, JJ
为了更全面地描述性激素对听性脑干反应（ABR）潜伏期的影响，我们评估了正常男性和女性受试者以及先前诊断为内分泌综合征的女性的ABR。我们描述了以下受试者的ABR潜伏期结果：五名正常男性，九名正常周期性女性，没有激素治疗，九名女性使用口服避孕药，五名女性患有卵巢早衰（POF），接受周期性雌激素-孕酮替代治疗，五名高雄激素化女性患有多囊卵巢疾病（PCOD），用促性腺激素释放激素激动剂Lupron Depot治疗，来抑制卵巢类固醇的产生所有受试者的年龄均在23至40岁之间。测量雌二醇、孕酮、睾酮、催乳素和促性腺激素（促黄体生成素和促卵泡激素）的血清水平，以记录ABR评价时每例受试者的激素状态。正常骑自行车的女性和女性POF进行ABR测试在同一周期的不同阶段。对使用避孕药的男性受试者和女性受试者进行了4次研究;基线，然后在Lupron贮库型药物治疗开始后间隔2周。ABR波V峰潜伏期增加与雌激素或睾酮水平升高有关。我们以前曾报道，在女性月经周期中，ABR波V峰潜伏期延长与雌激素峰值水平一致。由于睾酮通过中枢神经内分泌组织转化为雌激素，从而对脑功能产生影响，因此我们推测，男性的潜伏期增加是睾酮在中枢听觉通路中芳构化为雌激素的结果。这一假设可以解释在用Lupron治疗以抑制卵巢雄激素分泌之前，在睾酮升高的PCOD雌性动物中发现的V波峰值轻微增加。这些研究结果表明，神经传导时间修改的雌激素浓度的变化在脑干听觉通路的男女。
In an effort to characterize more completely the influence of sex hormones on auditory brainstem response (ABR) latency, we evaluated the ABRs of normal male and female subjects and women with previously diagnosed endocrinologic syndromes. We describe ABR latency results from the following subjects: five normal males, nine normally cycling females on no hormonal therapy, nine females using oral contraceptive pills, five females with premature ovarian failure (POF) undergoing cyclic estrogen-progesterone replacement therapy, and five hyperandrogenized females with polycystic ovarian disease (PCOD) treated with the gonadotropin-releasing hormone agonist, Lupron depot, to suppress ovarian steroid production. All subjects were between 23 and 40 years of age. Serum levels of estradiol, progesterone, testosterone, prolactic, and gonadotropins (lutienizing hormone and follicle stimulating hormone) were measured to document the hormonal status of each of the subjects at the time of the ABR evaluation. Normal cycling females and females with POF underwent ABR testing during different phases of the same cycle. Male subjects and females using birth control pills were studied four times; baseline and then at 2-week intervals after the initiation of Lupron depot therapy. Increased ABR wave V peak latencies were found to be associated with elevated levels of estrogen or testosterone. We have previously reported a lengthening of ABR wave V peak latencies coincident with peak estrogen levels during the female cycle. Because testosterone is converted to estrogen by central neuroendocrine tissue to exert its effect on brain function, we postulated that increased latency in males is a result of the effect of aromatization of testosterone to estrogen in the central auditory pathway. This hypothesis would account for the slightly increased wave V peak latencies found in the PCOD females with elevated testosterone before treatment with Lupron to suppress ovarian androgen secretion. These findings suggest that neural conduction time is modified by changes in estrogen concentrations in the brainstem auditory pathway of both sexes.