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首页> 外文期刊>The European Journal of Neuroscience >Rapid changes in hippocampal CA1 pyramidal cell function via pre- as well as postsynaptic membrane mineralocorticoid receptors.
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Rapid changes in hippocampal CA1 pyramidal cell function via pre- as well as postsynaptic membrane mineralocorticoid receptors.

机译：通过突触前和突触后膜盐皮质激素受体快速改变海马CA1锥体细胞功能。

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摘要

Corticosterone (100 nm) rapidly increases the frequency of miniature excitatory postsynaptic currents in mouse CA1 pyramidal neurons via membrane-located mineralocorticoid receptors (MRs). We now show that a presynaptic ERK1/2 signalling pathway mediates the nongenomic effect, as it was blocked by the MEK inhibitors U0126 (10 microm) and PD098059 (40 microm) and occluded in H-Ras(G12V)-mutant mice with constitutive activation of the ERK1/2 presynaptic pathway. Notably, the increase in mEPSC frequency was not mediated by retrograde signalling through endocannabinoids or nitric oxide, supporting presynaptic localization of the signalling pathway. Unexpectedly, corticosterone was also found to have a direct postsynaptic effect, rapidly decreasing the peak amplitude of I(A) currents. This effect takes place via postsynaptic membrane MRs coupled to a G protein-mediated pathway, as the effect of corticosterone on I(A) was effectively blocked by 0.5 mm GDP-beta-S administered via the recording pipette into the postsynaptic cell. Taken together, these results indicate that membrane MRs mediate rapid, nongenomic effects via pre- as well as postsynaptic pathways. Through these dual pathways, high corticosterone concentrations such as occur after stress could contribute to enhanced CA1 pyramidal excitability.
机译：皮质酮（100 nm）通过膜定位的盐皮质激素受体（MRs）快速增加小鼠CA1锥体神经元中小型兴奋性突触后突触电流的频率。我们现在显示突触前ERK1 / 2信号通路介导非基因组效应，因为它被MEK抑制剂U0126（10 microm）和PD098059（40 microm）阻断，并被H-Ras（G12V）突变型小鼠激活并闭塞的ERK1 / 2突触前通路。值得注意的是，mEPSC频率的增加不是由通过内源性大麻素或一氧化氮的逆行信号介导的，从而支持了信号通路的突触前定位。出乎意料的是，还发现皮质酮具有直接的突触后作用，迅速降低了I（A）电流的峰值幅度。这种作用是通过与G蛋白介导的途径耦合的突触后膜MR来实现的，因为皮质酮对I（A）的作用被通过记录移液管注入突触后细胞的0.5 mmGDP-β-S有效阻断。综上所述，这些结果表明膜MR通过突触前和突触后途径介导快速的非基因组效应。通过这些双重途径，高皮质酮浓度（例如在压力后发生）可能有助于增强CA1锥体兴奋性。

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