A NEUROGENIC TIMING FACTOR IN CONTROL OF THE OVULATORY DISCHARGE OF LUTEINIZING HORMONE IN THE CYCLIC RAT
A NEUROGENIC TIMING FACTOR IN CONTROL OF THE OVULATORY DISCHARGE OF LUTEINIZING HORMONE IN THE CYCLIC RAT
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DOI：
10.1210/endo-44-3-234
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发表时间：
1949-01-01
期刊：
影响因子：
4.8
通讯作者：
MARKEE, JE
中科院分区：
文献类型：
--
作者：
EVERETT, JW;SAWYER, CH;MARKEE, JE
双苯胺或阿托品可阻断雌激素损伤后促黄体生成素释放的机制。由于这些药物既不干扰激素的腺体分泌，也不干扰其对卵巢的作用，因此得出的结论是，雌激素影响促黄体生成素的释放至少部分是通过神经系统，可能是通过下丘脑。本报告论证了类似机制在周期大鼠中的存在及其与周期的时间关系，这与损伤的结果有关。在不同的时间注射二苯胺或阿托品。发情前期的那一天。除初步试验外，所用动物为68只4天周期的大鼠，属于一个品系，其排卵通常发生在发情前期的凌晨1-2：30之间。在注射二苯胺的时候。在下午2点或更早的发情前期，大多数情况下排卵被阻止或显著延迟。在这些时间注射阿托品可以均匀地防止排卵前肿胀或排卵。与任何一种药物的这些阻断作用相关的是，卵巢间质组织未能经历通常的胆固醇耗竭，而前一周期的黄体未能储存胆固醇。子宫通常在损伤后第二天仍保持扩张状态。在大多数情况下，阴道涂片序列明显延迟。在发情前期的下午4点，注射两种药物中的任何一种时，除了用二苯胺治疗的少数大鼠排卵迟缓外，排卵没有受到明显的干扰。在大多数情况下，唯一对黄体生成素释放有影响的迹象是黄体胆固醇储存的明显延迟。结论是，在这种品系的大鼠中，在我们的群体条件下，神经肌肉对腺垂体的刺激发生在发情前期，即下午2点至4点，10至12小时。排卵前。这种时序上有限的神经体液刺激对于黄体生成素的充分释放是必不可少的，这一证明清楚地提供了一种手段，通过这种手段，多性周期的各种特征可以与环境节律同步。
Dibenamine or atropine will block the mechanism which leads to release of LH from the adenohypophysis after estrogen injn. Since these drugs do not interfere with the glandular discharge of the hormone nor with its action on the ovary, the conclusion was reached that estrogen effects LH release at least partially by way of the nervous system, presumably the hypothalamus. The existance in the cyclic rat of a similar mechanism and the chronologic relationship of this to the cycle are demonstrated in the present report, which concerns the results of injns. of Dibenamine or of atropine at various hrs. of the day of proestrus. Excepting preliminary expts., the animals used were 68 4-day cyclic rats belonging to a strain in which ovulation normally occurs between 1 and 2:30 A.M. in the early morning after proestrus. When Dibenamine was injd. during proestrus at 2 P.M. or earlier, ovulation was prevented or significantly retarded in most cases. Injection of atropine at these hours uniformly prevented preovulatory swelling or ovulation. Associated with these blocking effects of either drug was the failure of both the ovarian interstitial tissue to undergo the usual cholesterol depletion and of the corpora lutea of the preceding cycle to store cholesterol. The uteri usually remained distended the day after injn. In most cases the vaginal smear sequence was retarded significantly. When either drug was injd, at 4 P.M. during proestrus, ovulation proceeded without detectable interference apart from retardation in a few rats treated with Dibenamine. In the majority of cases the only suggestion of an effect upon LH release was an apparent delay of luteal cholesterol storage. It is concluded that in this strain of rats, under our colony conditions, neurochumoral stimulation of the adenohypophysis occurs during proestrus between 2 and 4 P.M., 10-12 hrs. before ovulation. The demonstration that this chronologically limited neurohumoral stimulus is essential to adequate release of LH clearly offers a means by which various features of the polyestrous cycle may be synchronized with environmental rhythms.