Forman L J, Estilow S
Department of Medicine, University of Medicine and Dentistry of New Jersey, School of Osteopathic Medicine, Camden 08103.
Proc Soc Exp Biol Med. 1988 Feb;187(2):190-6. doi: 10.3181/00379727-187-42653.
Immunoreactive beta-endorphin (IR-BE) levels in the plasma, anterior pituitary (AP), the neurointermediate lobe of the pituitary (NIL), and the hypothalamus were determined in castrated female rats and castrated female rats treated with estradiol benzoate (estrogen), after exposure to acute (once for 45 min) or chronic (45 min each day for 15 consecutive days) immobilization stress. Acute and chronic stress increased plasma levels of IR-BE to the same extent in castrated female rats and castrated female rats treated with estrogen. In castrated female rats, acute stress produced an increase in the concentration of IR-BE in the AP, which was attenuated by the administration of estrogen. Although IR-BE in the NIL was not influenced by acute stress in castrated animals, exposure to acute stress resulted in an elevation in IR-BE levels in the NIL of rats given estrogen. Chronic stress did not affect the concentration of IR-BE in the AP of castrated females or castrated females treated with estrogen. Chronic stress did, however, increase the concentration of IR-BE in the NIL of castrated animals. This affect of stress on IR-BE levels in the NIL was potentiated by estrogen administration. IR-BE levels in the hypothalamus were reduced by estrogen and were not affected by acute or chronic stress, regardless of the gonadal steroid environment. As determined by column chromatography, administration of estrogen, as well as subjection to chronic stress, promoted the processing of the proopiomelanocortin precursor to form beta-lipotropin rather than beta-endorphin in the AP. By these methods, the only immunoreactivity detected in the NIL and the hypothalamus was beta-endorphin. These data indicate that IR-BE levels in the plasma, the AP, and the NIL of female rats are affected by immobilization stress and that estrogen modulates the effects of acute immobilization stress on IR-BE levels in the AP and the NIL and the effects of chronic immobilization stress on the levels of IR-BE in the NIL.
在去势雌性大鼠以及用苯甲酸雌二醇(雌激素)处理的去势雌性大鼠中,测定了在遭受急性(单次45分钟)或慢性(连续15天每天45分钟)固定应激后,血浆、垂体前叶(AP)、垂体神经中间叶(NIL)和下丘脑内免疫反应性β-内啡肽(IR-BE)的水平。急性和慢性应激使去势雌性大鼠和用雌激素处理的去势雌性大鼠的血浆IR-BE水平升高至相同程度。在去势雌性大鼠中,急性应激使AP中IR-BE的浓度增加,而雌激素给药可使其减弱。虽然去势动物的急性应激对NIL中的IR-BE没有影响,但急性应激导致给予雌激素的大鼠NIL中IR-BE水平升高。慢性应激对去势雌性大鼠或用雌激素处理的去势雌性大鼠的AP中IR-BE的浓度没有影响。然而,慢性应激确实增加了去势动物NIL中IR-BE的浓度。雌激素给药增强了应激对NIL中IR-BE水平的这种影响。下丘脑内的IR-BE水平因雌激素而降低,且不受急性或慢性应激的影响,无论性腺类固醇环境如何。通过柱色谱法测定,雌激素给药以及慢性应激均促进了阿片促黑激素原前体在AP中加工形成β-促脂素而非β-内啡肽。通过这些方法,在NIL和下丘脑中检测到的唯一免疫反应性是β-内啡肽。这些数据表明,雌性大鼠血浆、AP和NIL中的IR-BE水平受固定应激影响,且雌激素调节急性固定应激对AP和NIL中IR-BE水平的影响以及慢性固定应激对NIL中IR-BE水平的影响。