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首页> 外文期刊>The European Journal of Neuroscience >The forced swimming-induced behavioural immobility response involves histone H3 phospho-acetylation and c-Fos induction in dentate gyrus granule neurons via activation of the N-methyl-D-aspartate/extracellular signal-regulated kinase/mitogen- and stress-activated kinase signalling pathway
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The forced swimming-induced behavioural immobility response involves histone H3 phospho-acetylation and c-Fos induction in dentate gyrus granule neurons via activation of the N-methyl-D-aspartate/extracellular signal-regulated kinase/mitogen- and stress-activated kinase signalling pathway

机译：强迫游泳诱导的行为不动反应涉及通过激活N-甲基-D-天冬氨酸/细胞外信号调节激酶/促分裂原和应激激活激酶信号转导在齿状回颗粒神经元中的组蛋白H3磷酸乙酰化和c-Fos诱导通路

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摘要

The hippocampus is involved in learning and memory. Previously, we have shown that the acquisition of the behavioural immobility response after a forced swim experience is associated with chromatin modifications and transcriptional induction in dentate gyrus granule neurons. Given that both N-methyl-D-aspartate (NMDA) receptors and the extracellular signal-regulated kinases (ERK) 1/2 signalling pathway are involved in neuroplasticity processes underlying learning and memory, we investigated in rats and mice whether these signalling pathways regulate chromatin modifications and transcriptional events participating in the acquisition of the immobility response. We found that: (i) forced swimming evoked a transient increase in the number of phospho-acetylated histone H3-positive [P(Ser10)-Ac(Lys14)-H3(+)] neurons specifically in the middle and superficial aspects of the dentate gyrus granule cell layer; (ii) antagonism of NMDA receptors and inhibition of ERK1/2 signalling blocked forced swimming-induced histone H3 phospho-acetylation and the acquisition of the behavioural immobility response; (iii) double knockout (DKO) of the histone H3 kinase mitogen- and stress-activated kinases (MSK) 1/2 in mice completely abolished the forced swimming-induced increases in histone H3 phospho-acetylation and c-Fos induction in dentate granule neurons and the behavioural immobility response; (iv) blocking mineralocorticoid receptors, known not to be involved in behavioural immobility in the forced swim test, did not affect forced swimming-evoked histone H3 phospho-acetylation in dentate neurons; and (v) the pharmacological manipulations and gene deletions did not affect behaviour in the initial forced swim test. We conclude that the forced swimming-induced behavioural immobility response requires histone H3 phospho-acetylation and c-Fos induction in distinct dentate granule neurons through recruitment of the NMDA/ERK/MSK 1/2 pathway.
机译：海马参与学习和记忆。以前，我们已经表明，强迫游泳经历后行为不动反应的获得与齿状回颗粒神经元的染色质修饰和转录诱导有关。鉴于N-甲基-D-天冬氨酸（NMDA）受体和细胞外信号调节激酶（ERK）1/2信号通路均参与了学习和记忆的神经可塑性过程，我们在大鼠和小鼠中研究了这些信号通路是否调节染色质修饰和转录事件参与了固定性反应的获得。我们发现：（i）强迫游泳引起磷酸乙酰化组蛋白H3阳性[P（Ser10）-Ac（Lys14）-H3（+）]神经元的数量短暂增加，特别是在中，浅层。齿状回颗粒细胞层; （ii）NMDA受体的拮抗作用和ERK1 / 2信号的抑制阻止了强迫游泳诱导的组蛋白H3磷酸乙酰化和行为不动反应的获得; （iii）小鼠中组蛋白H3激酶有丝分裂原和应激激活激酶（MSK）1/2的双重敲除（DKO）完全消除了强迫游泳引起的齿状颗粒中组蛋白H3磷酸乙酰化和c-Fos诱导的增加神经元和行为不动反应; （iv）阻断已知在强迫游泳试验中不涉及行为不动的盐皮质激素受体，并不影响在齿状神经元中强迫游泳诱发的组蛋白H3磷酸乙酰化; （v）在最初的强迫游泳试验中，药理学操作和基因缺失不影响行为。我们得出的结论是，强迫游泳引起的行为不动反应需要通过募集NMDA / ERK / MSK 1/2途径在不同的齿状颗粒神经元中进行组蛋白H3磷酸乙酰化和c-Fos诱导。

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