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视前区的 kainic 酸损伤会改变青春期前雌性大鼠中雌激素的正反馈。

Kainic acid lesioning of the preoptic area alters positive feedback of estrogen in prepubertal female rats.

作者信息

Clough R W, Rodriguez-Sierra J F, Hoppe L B

出版信息

Biol Reprod. 1986 Dec;35(5):1269-76. doi: 10.1095/biolreprod35.5.1269.

DOI:10.1095/biolreprod35.5.1269
PMID:3828436
Abstract

Stereotaxic infusion of kainic acid (KA) was performed to induce intrinsic neural lesions of the preoptic area (POA) in 25-day-old female rats. After KA infusion, rats in Experiment 1 received 10 micrograms of estradiol benzoate (EB) administered subcutaneously to assess positive feedback of EB on release of luteinizing hormone (LH) from the pituitary gland. Rats were perfused for light microscopic (LM) or electron microscopic (EM) evaluation of the lesion site. Rats of Experiment 2 were allowed to develop until the appearance of vaginal opening (VO) after which time vaginal lavages were taken to monitor the cyclicity of the vaginal epithelium. At 50 days of age, the right ovary from each rat was removed, trimmed of fat, and weighed. At 60 days of age, the remaining ovary was removed to assess compensatory ovarian hypertrophy (COH). In Experiment 3, we investigated the effects of POA/KA-infusion on sexual behavior. Sex behavior tests were conducted at 48 h after EB during the dark phase of the light cycle. In Experiment 1, all the control and saline-infused rats exhibited the expected rise of plasma LH two days after estrogen injection while the POA/KA-infusion abolished the positive feedback effect of EB on LH release. Ultrastructural examination of the lesion site revealed that neurons were undergoing acute degeneration while axons and afferent terminals seen in the same fields of analysis were morphologically intact. Preoptic area/KA lesions caused a marked delay in the appearance of VO. Duration of this temporal delay in POA/KA-lesioned rats was approximately 4 days, or one vaginal cycle. The lesioned animals showed normal compensatory hypertrophy after unilateral ovariectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

对25日龄雌性大鼠进行立体定向注射海人酸(KA)以诱导视前区(POA)的内在神经损伤。注射KA后,实验1中的大鼠皮下注射10微克苯甲酸雌二醇(EB),以评估EB对垂体促黄体生成素(LH)释放的正反馈作用。对大鼠进行灌注以进行损伤部位的光学显微镜(LM)或电子显微镜(EM)评估。实验2中的大鼠任其发育至出现阴道开口(VO),之后进行阴道灌洗以监测阴道上皮的周期性变化。在50日龄时,切除每只大鼠的右侧卵巢,去除脂肪并称重。在60日龄时,切除剩余的卵巢以评估代偿性卵巢肥大(COH)。在实验3中,我们研究了POA/KA注射对性行为的影响。在光照周期的黑暗阶段,于注射EB后48小时进行性行为测试。在实验1中,所有对照和注射生理盐水的大鼠在注射雌激素两天后血浆LH均出现预期升高,而POA/KA注射消除了EB对LH释放的正反馈作用。损伤部位的超微结构检查显示神经元正在发生急性变性,而在同一分析视野中看到的轴突和传入终末在形态上完好无损。视前区/KA损伤导致VO出现明显延迟。POA/KA损伤大鼠的这种时间延迟持续约4天,即一个阴道周期。损伤动物在单侧卵巢切除术后表现出正常的代偿性肥大。(摘要截断于250字)

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