Piercy M, Shin S H
Neuroendocrinology. 1980 Oct;31(4):270-5. doi: 10.1159/000123087.
The differences in plasma prolactin concentration between normal and estradiol-implanted male rats were compared after treatment with 3 different stimulating agents of prolactin secretion [ether anesthesia, pimozide (a "specific' dopaminergic receptor blocking agent) and TRH] using conscious, free-moving rats implanted with permanent intra-atrial cannulae. It has recently been shown that ether stress raises the circulating prolactin concentration by stimulating PRF secretion. The ether stress elevated prolactin concentration from 100 to 400 ng/ml in the estradiol-implanted rat and from 10 to 40 ng/ml in the normal male. Thus, the ether stress elevated the prolactin concentration 4 times over the basal level in both normal male and estradiol-implanted male rats, implying that the physiological role of the PRF is not changed by the estradiol implantation. A bolus injection of pimozide (1 mg/kg) elevated the plasma prolactin concentration in both the normal and estradiol-implanted male with an initial surge followed by descent to a maintained plateau level. This plateau level in the estradiol-primed rat was 600 ng/ml and in the nonprimed male rat, 50 ng/ml. The ratio of the plateau concentration over the basal level was 4 times for both groups, suggesting that the physiological role of the PIF in the estradiol-implanted rat is not different from that in the normal male rat. It is known that TRH not only stimulates TSH secretion but will stimulate prolactin secretion as well. A very large dose (0.6 mg/kg) of TRH elevated prolactin concentration 6-fold in the estradiol-implanted rat but stimulate little prolactin secretion in the normal male rat. Since ether exposure appears to stimulate prolactin secretion in both estradiol-primed and non-primed male rats through PRF secretion, while TRH was not able to stimulate a significant amount of prolactin secretion in the normal male rat, we concluded that TRH acts to stimulate prolactin secretion in estradiol-primed rats but through a different mechanism than that operating for PRF.
使用植入永久性心房插管的清醒、自由活动的大鼠，在给予3种不同的催乳素分泌刺激剂（乙醚麻醉、匹莫齐特（一种“特异性”多巴胺能受体阻断剂）和促甲状腺激素释放激素（TRH））后，比较正常雄性大鼠和植入雌二醇的雄性大鼠血浆催乳素浓度的差异。最近的研究表明，乙醚应激通过刺激催乳素释放因子（PRF）的分泌来提高循环催乳素浓度。在植入雌二醇的大鼠中，乙醚应激使催乳素浓度从100 ng/ml升高到400 ng/ml，而在正常雄性大鼠中从10 ng/ml升高到40 ng/ml。因此，在正常雄性大鼠和植入雌二醇的雄性大鼠中，乙醚应激均使催乳素浓度比基础水平升高了4倍，这意味着雌二醇植入并未改变PRF的生理作用。静脉注射匹莫齐特（1 mg/kg）可使正常雄性大鼠和植入雌二醇的雄性大鼠的血浆催乳素浓度升高，起初有一个峰值，随后下降至维持的平台水平。在预先给予雌二醇的大鼠中，该平台水平为600 ng/ml，在未预先处理的雄性大鼠中为50 ng/ml。两组平台浓度与基础水平的比值均为4倍，这表明在植入雌二醇的大鼠中，催乳素抑制因子（PIF）的生理作用与正常雄性大鼠并无差异。已知TRH不仅能刺激促甲状腺激素（TSH）分泌，还能刺激催乳素分泌。大剂量（0.6 mg/kg）的TRH可使植入雌二醇的大鼠的催乳素浓度升高6倍，但对正常雄性大鼠的催乳素分泌刺激作用很小。由于乙醚暴露似乎通过PRF分泌刺激预先给予雌二醇和未预先处理的雄性大鼠的催乳素分泌，而TRH在正常雄性大鼠中无法刺激大量催乳素分泌，因此我们得出结论，TRH在预先给予雌二醇的大鼠中可刺激催乳素分泌，但通过与PRF不同的机制起作用。
