首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Enhancement of rat hippocampal long-term potentiation by 17 beta-estradiol involves mitogen-activated protein kinase-dependent and -independent components.
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Enhancement of rat hippocampal long-term potentiation by 17 beta-estradiol involves mitogen-activated protein kinase-dependent and -independent components.

机译:17β-雌二醇增强大鼠海马长时程增强涉及丝裂原活化蛋白激酶依赖性和非依赖性成分。

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摘要

To investigate if estrogen modulates long-term potentiation (LTP) via mitogen-activated protein kinase (MAPK) activation, in vitro hippocampal slices were used to induce LTP through extracellular field recordings. Slices perfused with 17beta-estradiol exhibited a significant enhancement of LTP (224+/-19%) compared with LTP in control slices (157+/-9%). In the presence of PD098059, 17beta-estradiol still produced a significant magnitude of LTP (131+/-7%), revealing the existence of p-MAPK-independent LTP mediated by 17beta-estradiol. Immunocytochemistry showed that 17beta-estradiol promoted a transient increase in nuclear translocation of p-MAPK. 17beta-estradiol induced the extracellular proteolysis of neural cell adhesion molecule in a p-MAPK-independent manner, indicating that 17beta-estradiol may act on synaptic remodeling. These results indicate that 17beta-estradiol might affect hippocampal synaptic plasticity in a way involving two separate pathways, which are MAPK-dependent and MAPK-independent.
机译:为了研究雌激素是否通过有丝分裂原激活的蛋白激酶(MAPK)激活来调节长期增强(LTP),使用体外海马切片通过细胞外场记录诱导LTP。与对照切片中的LTP(157 +/- 9%)相比,灌注17β-雌二醇的切片表现出LTP的显着增强(224 +/- 19%)。在PD098059的存在下,17β-雌二醇仍产生大量LTP(131 +/- 7%),表明存在由17β-雌二醇介导的不依赖p-MAPK的LTP。免疫细胞化学显示17β-雌二醇促进p-MAPK核转运的瞬时增加。 17β-雌二醇以独立于p-MAPK的方式诱导神经细胞粘附分子的细胞外蛋白水解,表明17β-雌二醇可能在突触重塑中起作用。这些结果表明17β-雌二醇可能以涉及两个独立途径的方式影响海马突触可塑性,这两个途径是MAPK依赖性和MAPK依赖性的。

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