Department of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Behav Brain Res. 2022 May 3;425:113810. doi: 10.1016/j.bbr.2022.113810. Epub 2022 Feb 19.
Early life adversity has been suggested to affect neuroendocrine responses to subsequent stressors and accordingly vulnerability for behavioral disorders. This is the first work to study the effects of maternal separation (MS) stress on the co-occurrence of depression and cognitive impairments along with hippocampal inflammatory response under chronic social defeat stress (CSDS) in young adult male rats. During the first two postnatal weeks, the male pups were either exposed to MS or left undisturbed with their mothers (Std). Subsequently, starting on postnatal day 50, the animals of each group were either left undisturbed in the standard group housing (Con) or underwent CSDS for three weeks. Totally, there were four groups (n = 10/group), namely Std-Con, Ms-Con, Std-CSDS, and MS-CSDS. Pup retrieval test was performed on daily basis from PND1 to PND14. During the last week of the CSDS exposure, in the light phase, the behavioral tests and the retro-orbital blood sampling were performed to assess basal plasma corticosterone levels. Afterwards, the hippocampus of the animals was removed to measure the interleukin 1β (IL-1β) content. Exposure to CSDS increased the plasma corticosterone levels and induced social avoidance along with memory deficit. Maternal separation intensified hippocampal IL-1β contents as well as the plasma corticosterone levels in response to CSDS. Meanwhile, it facilitated the spatial learning and potentiated resilience to social avoidance and memory deficit. In conclusion, although maternal separation increased the basal plasma corticosterone levels, it could facilitate the learning process and induce resilience to the onset of depression and memory deficit in response to CSDS, probably through the compensatory increase in maternal care and the induction of mild hippocampal inflammatory response.
早期生活逆境被认为会影响神经内分泌对随后应激源的反应,从而导致行为障碍的易感性。这是第一项研究母体分离 (MS) 应激对慢性社交挫败应激 (CSDS) 下年轻雄性大鼠抑郁和认知障碍共病以及海马炎症反应影响的工作。在出生后的前两周,雄性幼崽要么经历 MS 应激,要么与母亲一起不受干扰 (Std)。随后,从出生后第 50 天开始,每组动物要么在标准组饲养中不受干扰 (Con),要么接受 CSDS 应激 3 周。总共分为四组 (n=10/组),即 Std-Con、Ms-Con、Std-CSDS 和 MS-CSDS。从 PND1 到 PND14,每天进行幼崽回收测试。在 CSDS 暴露的最后一周,在光照阶段,进行行为测试和眶后采血,以评估基础血浆皮质酮水平。随后,取出动物的海马体以测量白细胞介素 1β (IL-1β) 含量。CSDS 暴露增加了血浆皮质酮水平,并诱导了社交回避和记忆缺陷。母体分离加剧了海马体中的 IL-1β 含量以及对 CSDS 的血浆皮质酮水平。同时,它促进了空间学习,并增强了对社交回避和记忆缺陷的适应能力。总之,尽管母体分离增加了基础血浆皮质酮水平,但它可以促进学习过程,并在 CSDS 下诱导对抑郁和记忆缺陷的适应能力,这可能是通过增加母性行为的补偿和诱导轻度海马炎症反应。