Estradiol Reverses a Calcium-Related Biomarker of Brain Aging in Female Rats

被引：35
作者：
Brewer, Lawrence D. [1 ]
Dowling, Amy L. S. [1 ]
Curran-Rauhut, Meredith A. [1 ]
Landfield, Philip W. [1 ]
Porter, Nada M. [1 ]
Blalock, Eric M. [1 ]
机构：
[1] Univ Kentucky, Dept Mol & Biomed Pharmacol, Lexington, KY 40536 USA
来源：
JOURNAL OF NEUROSCIENCE | 2009年 / 29卷 / 19期
基金：
美国国家卫生研究院;
关键词：
LONG-TERM POTENTIATION; CA1 PYRAMIDAL NEURONS; ESTROGEN-RECEPTOR-ALPHA; HIPPOCAMPAL SYNAPTIC PLASTICITY; DENDRITIC SPINE DENSITY; ELEMENT-BINDING PROTEIN; AGE-RELATED ENHANCEMENT; SUBUNIT MESSENGER-RNA; CA2+ CHANNEL CA(V)1.2; ALZHEIMERS-DISEASE;
D O I：
10.1523/JNEUROSCI.5253-08.2009
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
An increase in L-type voltage-gated calcium channel (LTCC) current is a prominent biomarker of brain aging and is believed to contribute to cognitive decline and vulnerability to neuropathologies. Studies examining age-related changes in LTCCs have focused primarily on males, although estrogen (17 beta-estradiol, E2) affects calcium-dependent activities associated with cognition. Therefore, to better understand brain aging in females, the effects of chronic E2 replacement on LTCC current activity in hippocampal neurons of young and aged ovariectomized rats were determined. The zipper slice preparation was used to expose cornu ammonis 1 (CA1) pyramidal neurons for recording LTCC currents using the cell-attached patch-clamp technique. We found that an age-related increase in LTCC current in neurons from control animals was prevented by E2 treatment. In addition, in situ hybridization revealed that within stratum pyramidale of the CA1 area, mRNA expression of the Ca(v)1.2 LTCC subunit, but not the Ca(v)1.3 subunit, was decreased in aged E2-treated rats. Thus, the reported benefits of E2 on cognition and neuronal health may be attributed, at least in part, to its age-related decrease in LTCC current.
引用
收藏
页码：6058 / 6067
页数：10
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