壓力有時(shí)讓人記憶更清楚,，有時(shí)卻讓人易忘事。英國一項(xiàng)最新研究表明,，壓力對于記憶是一把雙刃劍,。
英國愛丁堡大學(xué)等機(jī)構(gòu)的研究人員在美國新一期《神經(jīng)科學(xué)期刊》上報(bào)告說，他們對一些年紀(jì)較大而記憶力漸差的實(shí)驗(yàn)鼠進(jìn)行了壓力測試,，并隨后對這些實(shí)驗(yàn)鼠在迷宮中表現(xiàn)出的記憶力,，及其大腦中隨壓力而產(chǎn)生的激素——皮質(zhì)醇水平進(jìn)行了分析。
結(jié)果顯示,，實(shí)驗(yàn)鼠大腦中有兩種與皮質(zhì)醇有關(guān)的受體,，當(dāng)壓力較小時(shí)，較低的皮質(zhì)醇含量會(huì)激活其中一種受體,，這種受體的功能有助記憶；而當(dāng)壓力持續(xù)較大時(shí),，增多的皮質(zhì)醇含量超出了這種受體的接受范圍,，開始激活另一種受體,，而第二種受體的作用則會(huì)減弱記憶。
研究人員指出,，這一發(fā)現(xiàn)說明壓力對于記憶是一柄雙刃劍,，這解釋了為什么有時(shí)一點(diǎn)壓力能增強(qiáng)記憶，而長期壓力會(huì)減弱記憶的情況,。
研究人員還嘗試用藥物阻斷第二種受體的作用,，結(jié)果顯示這可以幫助實(shí)驗(yàn)鼠恢復(fù)一些記憶。如果能在此基礎(chǔ)上開發(fā)出適用于人類的藥物,，也許將有助于對老年癡呆癥等與記憶相關(guān)疾病的治療,。（生物谷Bioon.com）
生物谷推薦原文出處：
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.
