CENTRAL ADMINISTRATION OF CORTICOTROPIN-RELEASING FACTOR MODULATES OXYTOCIN SECRETION IN THE RAT
CENTRAL ADMINISTRATION OF CORTICOTROPIN-RELEASING FACTOR MODULATES OXYTOCIN SECRETION IN THE RAT
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DOI：
10.1210/endo-119-4-1558
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发表时间：
1986-10-01
期刊：
影响因子：
4.8
通讯作者：
VALE, WW
中科院分区：
文献类型：
--
作者：
BRUHN, TO;SUTTON, SW;VALE, WW
最近，有报道称，催产素（OT），其经典已知的功能在分娩和哺乳期，分泌的反应，应激刺激在雄性大鼠。在这些和本报告中，发现游泳应激、束缚应激、乙醚应激和足电击应激升高OT分泌而不影响精氨酸加压素（AVP）分泌。在目前的研究中，我们调查了可能的调制OT分泌的CRF，这是已知的压力过程中释放。雄性和雌性大鼠接受脑室内（icv）注射0.75nmol（5 μ g）大鼠CRF，并在处理后5分钟处死。CRF显着增加OT分泌的雄性和雌性大鼠分别为3.4和4倍。血浆AVP水平不受治疗影响。CRF对OT释放的影响是结构特异性的，因为大鼠CRF、绵羊CRF和suagvagine是OT的等效释放物，而绵羊CRF 7 -41是CRF的无活性类似物，不改变血浆OT水平。在另一组实验中，用CRF抗血清（0.5ml i.v）或地塞米松（20 μ g/大鼠ip）预处理大鼠，然后用icv CRF注射。CRF抗血清和地塞米松均能完全阻断icvCRF后ACTH释放的增加，但不影响OT反应。这表明CRF可能在中枢而不是在神经垂体水平上改变OT分泌。由于室旁核的小细胞神经元而不是大细胞神经元在免疫组织化学研究中已被证明是类固醇敏感的，我们建议CRF可能直接或间接作用于大细胞神经元以增加OT释放。静脉注射0.75 nmol CRF可使外周血OT和AVP水平升高。这种增加的幅度与icv给药CRF后的反应相似（2- 4倍刺激）。CRF静脉给药导致低血压，因此可能引起压力感受器介导的AVP和OT释放。结论：1）在不引起血容量和渗透压变化的生理和心理应激条件下，大鼠OT分泌增加，AVP分泌保持不变; 2）侧脑室注射CRF可模拟乙醚应激或足电击应激后的OT反应; 3）CRF可能在调节应激诱导的OT分泌中发挥作用。
Recently, it has been reported that oxytocin (OT), classically known for its function during parturition and lactation, is secreted in response to stressful stimuli in male rats. In these and in the present report it was found that swimming stress, restraint stress, ether stress, and footshock stress elevate OT secretion without affecting arginine-vasopressin (AVP) secretion. In the present studies, we investigated the possible modulation of OT secretion by CRF which is known to be released during stress. Male and female rats received intraventricular (icv) injections of 0.75 nmol (5 .mu.g) rat CRF and were killed 5 min after the treatment. CRF significantly elevated OT secretion in male and female rats 3.4- and 4-fold, respectively. Plasma AVP levels were not affected by the treatment. The effect of CRF on OT release was structure specific since rat CRF, ovine CRF, and suagvagine were equipotent releasers of OT while an inactive analog to CRF, ovine CRF7-41 did not change plasma OT levels. In another set of experiments rats were pretreated with either CRF-antiserum (0.5 ml i.v) or dexamethsone (20 .mu.g/rat ip) and then injected with icv CRF. Both CRF-antiserum and dexamethasone blocked the rise in ACTH release after icv CRF completely but did not influence the OT response. This suggests CRF may be acting centrally but not at the level of the neurohypophysis to change OT secretion. Since parvocelluar but not magnocellular neurons of the paraventricular nucleus have been demonstrated to be steroid sensitive in immunohistochemical studies, we suggest CRF may act directly or indirectly upon magnocellular neurons to increase OT release. Intravenous administration of 0.75 nmol CRF increased both OT and AVP levels in peripheral blood. The magnitude of this increase was similar (2- to 4-fold stimulation) to responses after icv administration of CRF. Intravenous administration of CRF results in hypotension and may therefore cause a baroreceptor mediated release of AVP and OT. From the above evidence we conclude: 1) physical and mental stresses which do not result in changes in blood volume or osmolality evoke an increase in OT secretion while AVP secretion remains unchanged; 2) CRF administered icv mimics OT responses observed after ether stress or footshock stress: 3) CRF may play a role in regulating stress-induced OT secretion in the rat.