Corticosterone binding to hippocampus: immediate and delayed influences of the absence of adrenal secretion.
Corticosterone binding to hippocampus: immediate and delayed influences of the absence of adrenal secretion.
复制标题
皮质酮与海马体的结合：肾上腺分泌缺乏的直接和延迟影响。
DOI：
10.1016/0006-8993(74)90321-7
复制
发表时间：
1974
期刊：
影响因子：
2.9
通讯作者：
C. Magnus
中科院分区：
文献类型：
--
作者：
B. McEwen;G. Wallach;C. Magnus
研究了[3H]皮质酮与大鼠脑海马中可溶性（细胞质）和细胞核结合位点的结合与内源性皮质酮分泌的存在或短期和长期缺乏的关系。 (1) 在正常大鼠体内可检测到饱和结合，但内源性激素，包括注射[3H]皮质酮应激引起的分泌，可以通过竞争结合位点和从结合位点取代结合激素来干扰体内结合的测量。 (2)双侧肾上腺切除术后，随着内源性皮质酮水平下降，体内可用皮质酮结合位点在长达2小时内迅速增加，随后总结合能力长期增加，并在术后几天内达到平台状态。 (3)组织切片中的海马细胞核和海马匀浆中的胞质结合蛋白对[3H]皮质酮摄取的体外研究也显示了两种肾上腺切除术后的增加。第二次增加在肾上腺切除术后11小时以上开始，因此手术后2或11小时的[3H]皮质酮结合能力似乎反映了在没有内源性激素的情况下完整大鼠的能力。 (4)甲状腺切除术和垂体切除术可以防止肾上腺切除术后血清皮质酮结合活性的增加，但不能阻止海马皮质酮结合的增加。 (5) 在体内和体外，在细胞质和细胞核部分都发现海马结合能力的长期增加。因此，虽然控制激素进入细胞核的单独机制是完全可能的，但不需要它们来解释目前的结果。 (6)在肾上腺切除的大鼠中，海马细胞核结合位点半最大饱和的皮质酮体内剂量估计约为15μg。该剂量在注射后 10 分钟产生血清皮质酮水平，该水平处于正常大鼠早晨静息皮质酮水平的范围内。结论是海马皮质酮结合系统在内源性皮质酮的正常每日范围内运行。
Binding of [3H]corticosterone to soluble (cytosol) and cell nuclear binding sites in hippocampus of rat brain was studied in relationship to the presence or the short-term and long-term absence of endogenous corticosterone secretion. (1) Saturable binding is detectablein vivoin normal rats, but endogenous hormone, including secretion evoked by stress of injecting [3H]corticosterone, can interfere with measurement of bindingin vivoby both competing for binding sites and displacing bound hormone from binding sites. (2) After bilateral adrenalectomy, there is a rapid increase in availablein vivocorticosterone binding sites for up to 2 h, as endogenous corticosterone levels fall, followed by a longer-term increase in total binding capacity which approaches a plateau over several days after the operation. (3)In vitrostudies of uptake of [3H]corticosterone both to hippocampal cell nuclei in tissue slices and to cytosol binding proteins in hippocampal homogenates also show the two post-adrenalectomy increases. The second increase begins more than 11 h after adrenalectomy, so that [3H]corticosterone binding capacity either 2 or 11 h after the operation appears to reflect the capacity in intact rats in the absence of endogenous hormone. (4) Thyroidectomy and hypophysectomy, which prevent increases in serum corticosterone binding activity which follows adrenalectomy, fail to block increases in hippocampal corticosterone binding. (5) Long-term increases in hippocampal binding capacity are foundin vivoas well asin vitroin both the cytosol and cell nuclear fractions. Thus, while separate mechanisms governing entry of the hormone into the cell nuclei are entirely possible, they are not required to explain the present results. (6) Thein vivodose of corticosterone in adrenalectomized rats which half-maximally saturated the hippocampal cell nuclear binding sites is estimated to be around 15 μg. This dose produces serum corticosterone levels at 10 min after injection which are in the range of resting morning levels of corticosterone in normal rats. It is concluded that the hippocampal corticosterone binding system operates within the normal daily range of endogenous corticosterone.