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慢性社会隔离对 HPA 轴适应异型应激的影响。

Chronic social isolation in adaptation of HPA axis to heterotypic stress.

机构信息

Department of Physiology, Institute of Pharmacology, Polish Academy of Sciences, Kraków, Poland.

Department of Pathophysiology, Jagiellonian University Medical College, Kraków, Poland.

出版信息

Pharmacol Rep. 2017 Dec;69(6):1213-1223. doi: 10.1016/j.pharep.2017.08.011. Epub 2017 Nov 10.

DOI:10.1016/j.pharep.2017.08.011
PMID:29128802
Abstract

BACKGROUND

Social crowding and isolation are recognized as major stressors and risk factors for development of psychiatric disorders. Chronic isolation stress (IS) and crowding stress (CS) activate neuroendocrine and neurochemical mechanisms, that activate the hypothalamic-pituitary-adrenal (HPA) axis. Changes of the plasma level of interleukin-1β (IL-1β), ACTH and corticosterone (CORT) after chronic psychosocial IS and CS were investigated.

METHODS

Control rats were kept 5 per cage and not stressed. Stressed groups were subjected to either CS for 3, 7, 14days+restraint stress (RS) or IS for (11days) before this treatment was applied. Crowded rats were remained (24 in one cage) and RS rats were restrained for 10min. Total CORT, ACTH and IL-1β levels were measured using commercially available kits.

RESULTS

Social CS for 3days significantly increased plasma IL-1β level. Social IS increased plasma IL-1β level after longer period of subsequent CS 7 and 14days, than ACTH and CORT, after 3 and 7days. Prior IS significantly increased plasma IL-1β level induced by subsequent combined CS for 3days+acute RS, but significantly or totally inhibited the acute stress-induced increase of plasma IL-1β level after 7 and 14days of combined stress. IS, by contrast, strongly inhibited the increase of plasma ACTH and CORT level induced by combined CS+acute RS.

CONCLUSION

Chronic IS augments the changes of IL-1β level induced by a longer crowding period than ACTH and CORT. Modulatory action of IL-1β and pituitary-adrenocortical hormones adaptation to chronic social stress is asynchronous.

摘要

背景

社会拥挤和隔离被认为是精神疾病发展的主要应激源和危险因素。慢性隔离应激(IS)和拥挤应激(CS)激活神经内分泌和神经化学机制,激活下丘脑-垂体-肾上腺(HPA)轴。研究了慢性社会 IS 和 CS 后白细胞介素-1β(IL-1β)、促肾上腺皮质激素(ACTH)和皮质酮(CORT)血浆水平的变化。

方法

对照组大鼠每笼饲养 5 只,不受压力。应激组分别接受 CS(3、7、14 天+束缚应激(RS)或 IS(11 天)处理。拥挤的大鼠被保留(一个笼子里 24 只),RS 大鼠被束缚 10 分钟。使用市售试剂盒测量总 CORT、ACTH 和 IL-1β 水平。

结果

社会 CS 3 天显著增加了血浆 IL-1β 水平。社会 IS 在更长时间的后续 CS 7 和 14 天后增加了血浆 IL-1β 水平,而 ACTH 和 CORT 在 3 和 7 天后增加。先前的 IS 显著增加了随后 3 天+急性 RS 联合 CS 诱导的血浆 IL-1β 水平,但显著或完全抑制了 7 和 14 天联合应激后急性应激诱导的血浆 IL-1β 水平增加。相比之下,IS 强烈抑制了联合 CS+急性 RS 诱导的血浆 ACTH 和 CORT 水平的增加。

结论

慢性 IS 增强了 IL-1β 水平的变化,比 ACTH 和 CORT 更长的拥挤期诱导。IL-1β 和垂体肾上腺皮质激素对慢性社会应激的调节作用是不同步的。

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