Briski K, Quigley K, Meites J
Proc Soc Exp Biol Med. 1984 Nov;177(2):354-9. doi: 10.3181/00379727-177-41956.
The purpose of the present study was to examine the effect of administering an opiate receptor antagonist, naltrexone (NALT) on the decline in pituitary thyrotropin (TSH) release induced by both acute and chronic stress, and to determine whether norepinephrine (NE) is involved in the mechanism by which opiate receptor blockade counteracts inhibition of TSH release during stress. Administration of NALT, a specific opiate receptor antagonist, significantly attenuated the decrease in plasma TSH observed after acute exposure to ether or restraint stress. The ability of NALT to prevent suppression of circulating TSH in ether-stressed rats was blocked by pharmacological suppression of NE activity induced by pretreatment with diethyldithiocarbamate (DDC) or phenoxybenzamine (PB), both NE antagonists. In chronically stressed rats, thrice daily injections of NALT attenuated the sustained decline in circulating TSH, and resulted in a significant elevation in plasma TSH when compared with stressed, saline-treated animals. Pretreatment with DDC prior to NALT injection abolished this stimulatory effect of NALT. These observations indicate that opiate/receptor interaction is prerequisite for the decrease in circulating TSH release during both acute and chronic stress, and support the hypothesis that endogenous opioid peptides (EOPs) mediate the suppressive effect of stress on TSH release. The finding that uninterrupted NE function is necessary for NALT's action on TSH release during stress suggests that the suppressive effect of stress on TSH and its reversal by opiate antagonists involves alterations in hypothalamic NE activity.
本研究的目的是检验给予阿片受体拮抗剂纳曲酮（NALT）对急性和慢性应激诱导的垂体促甲状腺激素（TSH）释放下降的影响，并确定去甲肾上腺素（NE）是否参与阿片受体阻断在应激期间抵消TSH释放抑制作用的机制。给予特异性阿片受体拮抗剂NALT，可显著减轻急性暴露于乙醚或束缚应激后观察到的血浆TSH下降。在乙醚应激大鼠中，NALT预防循环TSH抑制的能力被二乙基二硫代氨基甲酸盐（DDC）或苯氧苄胺（PB）预处理诱导的NE活性药理学抑制所阻断，这两种都是NE拮抗剂。在慢性应激大鼠中，每日三次注射NALT可减轻循环TSH的持续下降，与应激生理盐水处理的动物相比，血浆TSH显著升高。在注射NALT之前用DDC预处理消除了NALT的这种刺激作用。这些观察结果表明，阿片/受体相互作用是急性和慢性应激期间循环TSH释放减少的先决条件，并支持内源性阿片肽（EOPs）介导应激对TSH释放抑制作用的假说。应激期间NALT对TSH释放起作用需要不间断的NE功能这一发现表明，应激对TSH的抑制作用及其被阿片拮抗剂逆转涉及下丘脑NE活性的改变。
