Steroid-independent endogenous opioid peptide suppression of pulsatile luteinizing hormone release between estrus and diestrus in the rat estrous cycle.
Steroid-independent endogenous opioid peptide suppression of pulsatile luteinizing hormone release between estrus and diestrus in the rat estrous cycle.
复制标题
不依赖类固醇的内源性阿片肽抑制大鼠动情周期中动情期和动情间期之间的脉动黄体生成激素释放。
DOI：
10.1016/0006-8993(87)90902-4
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发表时间：
1987
期刊：
影响因子：
2.9
通讯作者：
Gallo,RV
中科院分区：
文献类型：
--
作者：
Babu,GN;Marco,J;Bona-Gallo,A;Gallo,RV
我们以前已经证明了在大鼠发情周期中，在发情期和间情期早期（D1）之间，卵巢类固醇激素对脉冲式促黄体生成激素（LH）释放的负反馈作用的缺失。本研究的目的是确定是否有类固醇非依赖性内源性阿片肽（EOP）抑制脉冲式LH释放在这同一24小时的时间间隔，如果是这样的话，脉冲式LH释放的参数（S）受到影响。大鼠在发情期、假卵巢切除术（OVX）后24 h或发情期08.30-10.00 h OVX时流血的。出血时，所有大鼠均静脉输注0.9%生理盐水（0.5 ml/h）或纳洛酮（0.005、0.05、0.5或2 mg/kg/h）4小时。输注开始后1 h，在09.30 - 12.30 h之间对大鼠流血的3 h（40或50 μl全血/5 min）。由于LH脉冲幅度和频率的增加，平均血液LH水平在发情期和D1早期之间增加。动情期OVX降低血浆雌二醇和孕酮水平24小时后，但没有增加脉冲LH释放的增加。然而，纳洛酮输注增强了假卵巢切除大鼠的脉冲式LH分泌的增加，呈剂量依赖性。虽然输注0.005或0.05 mg/kg/h没有影响，但0.5或2 mg/kg/h通过增加LH脉冲幅度和频率增加血液LH水平。同时注入吗啡可阻断纳洛酮对LH脉冲性释放的刺激作用，表明这种作用是由EOP受体介导的。此外，垂体对LHRH的反应性在体内没有改变纳洛酮输注，表明EOP受体拮抗剂的作用的中心网站。这些数据证实了我们以前的报告，即从发情到D1早期LH脉冲幅度和频率的增加发生在卵巢类固醇负反馈缺失的情况下。然而，脉冲式LH释放将进一步增加，在这一时间间隔，它不是一个集中发生的，类固醇独立的EOP抑制LH脉冲幅度和频率在这24小时期间的大鼠发情周期的存在。
We have previously demonstrated an absence of ovarian steroid negative feedback on pulsatile luteinizing hormone (LH) release between estrus and early diestrus 1 (D1) in the rat estrous cycle. The object of the present study was to determine if there was a steroid-independent endogenous opioid peptide (EOP) suppression of pulsatile LH release in thes same 24-h interval, and if so, which parameter(s) of pulsatile LH release were affected. Rats were bled on estrus, or 24 h following sham ovariectomy (OVX), or OVX at 08.30–10.00 h on estrus. At the time of bleeding all rats were infused i.v. for 4 h either with 0.9% saline (0.5 ml/h) or naloxone (0.005, 0.05, 0.5, or 2 mg/kg/h). At 1 h after the infusion began, rats were bled for 3 h (40 or 50 μl whole blood/5 min) between 09.30 and 12.30 h. Mean blood LH levels increased between estrus and early D1 due to increases in LH pulse amplitude and frequency. OVX on estrus decreased plasma levels of estradiol and progesterone 24 h later, but did not augment the increase in pulsatile LH release. However, naloxone infusion augmented the increase in pulsatile LH secretion in sham ovariectomized rats in a dose-dependent fashion. While infusion of 0.005 or 0.05 mg/kg/h had no effect, 0.5 or 2 mg/kg/h increased blood LH levels by increasing both LH pulse amplitude and frequency. The stimulatory effect of naloxone on pulsatile LH release was blocked by simultaneous infusion of morphine, demonstrating that the effect was mediated by EOP receptors. In addition, pituitary responsiveness to LHRH in vivo was not altered by naloxone infusion, indicating a central site of action for the EOP receptor antagonist. These data confirm our previous report that the increases in LH pulse amplitude and frequency occuring from estrus to early D1 occur in the absence of ovarian steroid negative feedback. However, pulsatile LH release would increase even further in this time interval were it not for the existence of a centrally occurring, steroid-independent EOP suppression of both LH pulse amplitude and frequency during this 24-h period of the rat estrous cycle.