Laboratory for Molecular Biology and Endocrinology, Institute of Nuclear Sciences "Vinča", University of Belgrade, P.O. Box 522-090, 11001 Belgrade, Serbia.
Neuroscience. 2013 Apr 16;236:47-54. doi: 10.1016/j.neuroscience.2013.01.033. Epub 2013 Jan 25.
The hippocampus plays a central role in stress-related mood disorders. The effects of acute vs. chronic stress on the integrity of hippocampal circuitry in influencing the vulnerability to, or resiliency against, neuronal injury are poorly understood. Here we investigated whether acute vs. chronic psychosocial isolation stress or a combination of the two (chronic stress followed by acute stress) influences the expression of the interneuronal marker parvalbumin (PV) and the chaperone-inducible heat shock protein 70 (Hsp70i) in different subregions of the hippocampus. Low levels of the Ca(2+)-binding protein (PV) may increase the vulnerability to neuronal injury, and Hsp70i represents an indicator of intense excitation-induced neuronal stress. Adult male Wistar rats were exposed to 2h of immobilization (IM) or cold (4°C) (acute stressors), 21d of social isolation (chronic stress), or a combination of both acute and chronic stress. Both chronic isolation and the combined stressors strongly decreased the PV-immunoreactive cells in the CA1, CA3 and dentate gyrus (DG) region of the hippocampus, while acute stress did not affect PV expression. The combination of acute and chronic stress induced a dramatic increase in Hsp70i expression in the DG, but Hsp70i expression was unaffected in acute and chronic stress alone. We also monitored serum corticosterone (CORT) levels as a neuroendocrine marker of the stress response. Acute stress increased CORT levels, while chronic isolation stress compromised hypothalamic-pituitary-adrenocortical (HPA) axis activity such that the normal stress response was impaired following subsequent acute stress. These results indicate that in contrast to acute stress, chronic isolation compromises the HPA axis and generates a considerable reduction in PV expression, representing a decrease in the calcium-buffering capacity and a putatively higher vulnerability of specific hippocampal interneurons to excitotoxic injury. The induction of Hsp70i expression in response to acute and chronic isolation reveals that neurons in the DG are particularly vulnerable to an acute stressor following a chronic perturbation of HPA activity.
海马体在与应激相关的情绪障碍中起着核心作用。急性应激与慢性应激对海马回路完整性的影响,进而影响神经元损伤的易感性或弹性,这方面的了解还很有限。在这里,我们研究了急性与慢性心理社会隔离应激,或两者的组合(慢性应激后紧接着急性应激)是否会影响海马体不同区域内中间神经元标志物钙结合蛋白(PV)和热休克蛋白 70(Hsp70i)的表达。钙结合蛋白(PV)水平较低可能会增加神经元损伤的易感性,而 Hsp70i 则代表强烈兴奋诱导的神经元应激的一个指标。成年雄性 Wistar 大鼠接受 2 小时的固定(IM)或冷(4°C)(急性应激源)、21 天的社会隔离(慢性应激)或两者的组合处理。慢性隔离和联合应激源强烈降低了海马体 CA1、CA3 和齿状回(DG)区域的 PV 免疫反应细胞,而急性应激源则不影响 PV 的表达。急性和慢性应激的组合在 DG 中诱导了 Hsp70i 表达的显著增加,而急性和慢性应激本身则不影响 Hsp70i 的表达。我们还监测了血清皮质酮(CORT)水平作为应激反应的神经内分泌标志物。急性应激会增加 CORT 水平,而慢性隔离应激会损害下丘脑-垂体-肾上腺皮质(HPA)轴的活动,使得随后的急性应激反应受损。这些结果表明,与急性应激不同,慢性隔离会损害 HPA 轴,并导致 PV 表达显著减少,这代表着钙缓冲能力下降,以及特定海马体中间神经元对兴奋性损伤的易感性增加。DG 中 Hsp70i 表达的诱导表明,在 HPA 活动慢性紊乱后,神经元对急性应激原特别敏感。