变慢性应激大鼠丘脑前嗅核对垂体-肾上腺轴和心脏β受体的影响。

M Suárez, P Paglini, R Fernández, J Enders, M Maglianesi, N Perassi, J Palma
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摘要

在基础和应激条件下,边缘结构在神经内分泌和交感肾上腺功能的控制中起重要作用。本研究旨在评价丘脑前核(ADTN)损伤大鼠血浆ACTH、肾上腺皮质活性、心脏肾上腺素受体密度和对可变慢性应激(VCS)的亲和力反应。病变后30 d,假面损伤应激动物血浆ACTH和皮质酮较假面损伤未应激动物升高(p < 0.05);损伤大鼠与未损伤大鼠相比,VCS后ACTH水平升高(p < 0.05)。在假性损伤动物中,应激后血浆皮质酮(C)升高,而在损伤动物中,与未受应激损伤的动物相比,C保持不变。应激组大鼠肾上腺C含量低于非应激组大鼠。在所有实验组中,β受体亲和力相似,但与基础组和损伤组相比,VCS假损伤动物的心脏d -肾上腺素能受体密度显著增加(P < 0.001)。我们的研究结果将证明心脏β肾上腺素受体密度的增加是由于慢性应激情况引起的ACTH、血浆皮质酮和交感神经反应的增加。ADTN病变减弱了这种海马肾上腺系统对慢性应激的反应以及上述心脏β肾上腺素受体密度的增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Influence of anterodorsal thalamic nuclei on the hypophyseal-adrenal axis and cardiac beta receptors in rats submitted to variable chronic stress.

The limbic structures play an important role in the control of the neuroendocrine and sympathical adrenal function in basal and stress conditions. This work was undertaken to evaluate plasma ACTH, adrenocortical activity, cardiac adrenoceptors density and affinity response to variable chronic stress (VCS) in anterodorsal thalamic nuclei (ADTN) lesioned rats. Thirty days after lesion, shamlesioned stressed animals increased plasma ACTH and corticosterone as compared to sham-lesioned unstressed animals (p < 0.05); lesioned rats increased ACTH levels after VCS (p < 0.05) as compared to unstressed-lesioned rats. Whereas in sham-lesion plasma corticosterone (C) increased after stress, in lesioned animals(C) remained unchanged as compared to unstressed-lesioned animals. In the stressed groups, adrenal C contents were below those found in unstressed rats. beta-receptors affinity, in all the experimental groups, was similar, but VCS sham-lesioned animals underwent a significant increase in cardiac D-adrenergic receptors density when compared with basal and lesioned groups (P < 0.001). Our findings would demonstrate that the increment in cardiac beta adrenoceptors density appears as a consequence of the increase in ACTH, plasma corticosterone and sympathetic response provoked by chronic stress situations. ADTN lesion attenuated this hipophisoadrenal system response to chronic stress as well as the above mentioned cardiac beta adrenoceptors density increment.

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