压力有时让人记忆更清楚,有时却让人易忘事。英国一项最新研究表明,压力对于记忆是一把双刃剑。
英国爱丁堡大学等机构的研究人员在美国新一期《神经科学期刊》上报告说,他们对一些年纪较大而记忆力渐差的实验鼠进行了压力测试,并随后对这些实验鼠在迷宫中表现出的记忆力,及其大脑中随压力而产生的激素——皮质醇水平进行了分析。
结果显示,实验鼠大脑中有两种与皮质醇有关的受体,当压力较小时,较低的皮质醇含量会激活其中一种受体,这种受体的功能有助记忆;而当压力持续较大时,增多的皮质醇含量超出了这种受体的接受范围,开始激活另一种受体,而第二种受体的作用则会减弱记忆。
研究人员指出,这一发现说明压力对于记忆是一柄双刃剑,这解释了为什么有时一点压力能增强记忆,而长期压力会减弱记忆的情况。
研究人员还尝试用药物阻断第二种受体的作用,结果显示这可以帮助实验鼠恢复一些记忆。如果能在此基础上开发出适用于人类的药物,也许将有助于对老年痴呆症等与记忆相关疾病的治疗。(生物谷Bioon.com)
生物谷推荐原文出处:
The Journal of Neuroscience, 16 March 2011, 31(11): 4188-4193; doi: 10.1523/?JNEUROSCI.6145-10.2011
11β-Hydroxysteroid Dehydrogenase Type 1 Deficiency Prevents Memory Deficits with Aging by Switching from Glucocorticoid Receptor to Mineralocorticoid Receptor-Mediated Cognitive Control
Joyce L. W. Yau1,2, June Noble2, and Jonathan R. Seckl1,2
Local brain amplification of glucocorticoids (GCs) by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) plays a pivotal role in age-related memory deficits. 11β-HSD1 deficient mice are protected from spatial memory impairments with aging, but the underlying mechanisms are unknown. To determine which brain receptors [high-affinity mineralocorticoid receptors (MRs) or low-affinity glucocorticoid receptors (GRs)] are involved, spatial memory was measured in aged 11β-HSD1?/? mice before and during intracerebroventricular infusion (10 d) of spironolactone (MR antagonist) or RU486 (GR antagonist). Aged C57BL/6J control mice showed impaired spatial memory in the Y-maze; this improved with GR blockade, while MR blockade had no effect. In contrast, aged 11β-HSD1?/? mice showed intact spatial memory that became impaired with MR blockade, but not GR blockade. Hippocampal MR and GR mRNA expression and plasma corticosterone levels were not significantly altered with spironolactone or RU486 in either genotype. These data support the notion that 11β-HSD1 deficiency in aging mice leads to lower intracellular GC concentrations in brain, particularly in the hippocampus, which activate predominantly MRs to enhance memory, while in aging C57BL/6J controls, the increased intracellular GCs saturate MRs and activate predominantly GRs, thus impairing memory, an effect reversed by GR blockade.