Yau Joyce L W, Noble June, Kenyon Christopher J, Ludwig Mike, Seckl Jonathan R
Centre for Cognitive Aging and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK; Endocrinology Unit, BHF Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK.
Eur J Neurosci. 2015 Mar;41(6):787-92. doi: 10.1111/ejn.12836. Epub 2015 Jan 23.
11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) locally regenerates active glucocorticoids from their inert forms thereby amplifying intracellular levels within target tissues including the brain. We previously showed greater increases in intra-hippocampal corticosterone (CORT) levels upon Y-maze testing in aged wild-type than in 11β-HSD1(-/-) mice coinciding with impaired and intact spatial memory, respectively. Here we examined whether ageing influences 11β-HSD1 regulation of CORT in the dorsal hippocampus under basal conditions during the diurnal cycle and following stress. Intra-hippocampal CORT levels measured by in vivo microdialysis in freely behaving wild-type mice displayed a diurnal variation with peak levels in the evening that were significantly elevated with ageing. In contrast, the diurnal rise in intra-hippocampal CORT levels was greatly diminished in 11β-HSD1(-/-) mice and there was no rise with ageing; basal intra-hippocampal CORT levels were similar to wild-type controls. Furthermore, a short (3 min) swim stress induced a longer lasting increase in intra-hippocampal CORT levels in wild-type mice than in 11β-HSD1(-/-) mice despite no genotypic differences in elevation of plasma CORT. These data indicate that 11β-HSD1 activity contributes substantially to diurnal and stress-induced increases in hippocampal CORT levels. This contribution is even greater with ageing. Thus, 11β-HSD1 inhibition may be an attractive target for treating cognitive impairments associated with stress or ageing.
11β-羟基类固醇脱氢酶1型(11β-HSD1)可将惰性糖皮质激素在局部再生为活性形式,从而提高包括大脑在内的靶组织内的细胞内水平。我们之前发现,在Y迷宫测试中,老年野生型小鼠海马内皮质酮(CORT)水平的升高幅度大于11β-HSD1基因敲除(-/-)小鼠,分别与受损和完整的空间记忆相对应。在此,我们研究了衰老是否会影响基础条件下、昼夜周期以及应激后背侧海马中11β-HSD1对CORT的调节。通过对自由活动的野生型小鼠进行体内微透析测量海马内CORT水平,发现其呈现昼夜变化,傍晚达到峰值水平,且随着衰老显著升高。相比之下,11β-HSD1基因敲除(-/-)小鼠海马内CORT水平的昼夜升高幅度大大减小,且不会随着衰老而升高;基础海马内CORT水平与野生型对照组相似。此外,尽管血浆CORT升高无基因型差异,但短时间(3分钟)游泳应激在野生型小鼠中诱导的海马内CORT水平升高持续时间比11β-HSD1基因敲除(-/-)小鼠更长。这些数据表明,11β-HSD1活性对海马CORT水平的昼夜变化和应激诱导升高有很大贡献。随着衰老,这种贡献更大。因此,抑制11β-HSD1可能是治疗与应激或衰老相关的认知障碍的一个有吸引力的靶点。