Aim

Oxytocin, a peptide hormone synthesized in the hypothalamic paraventricular nucleus, has been reported to participate in the regulation of learning and memory performance. However, no report has demonstrated the effect of oxytocin on the amyloid-beta (Aβ)-induced impairment of synaptic plasticity. In this study, we examined the effects of oxytocin on the Aβ-induced impairment of synaptic plasticity in mice.

Methods

To investigate the effect of oxytocin on synaptic plasticity, we prepared acute hippocampal slices for extracellular recording and assessed long-term potentiation (LTP) with perfusion of the Aβ active fragment (Aβ_25-35) in the absence and presence of oxytocin.

Results

We found that oxytocin reversed the impairment of LTP induced by Aβ_25-35 perfusion in the mouse hippocampus. These effects were blocked by pretreatment with the selective oxytocin receptor antagonist L-368,899. Furthermore, the treatment with the ERK inhibitor U0126 and selective Ca²⁺-permeable AMPA receptor antagonist NASPM completely antagonized the effects of oxytocin.

Conclusion

This is the first report to demonstrate that oxytocin could reverse the effects of Aβ on hippocampal LTP in mice. We propose that ERK phosphorylation and Ca²⁺-permeable AMPA receptors are involved in this effect of oxytocin.

中文翻译：

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催产素逆转了Aβ诱导的小鼠海马突触可塑性受损。

目标

催产素是一种在下丘脑室旁核中合成的肽激素，据报道参与学习和记忆性能的调节。但是，没有报道显示催产素对淀粉样蛋白（Aβ）诱导的突触可塑性损害的影响。在这项研究中，我们检查了催产素对Aβ诱导的小鼠突触可塑性损害的影响。

方法

为了研究对突触可塑性催产素的作用，我们制备了用于细胞外记录急性海马切片和评估长时程增强（LTP）与Aβ活性片段的灌注（Aβ _{25 - 35}）在不存在和催产素的存在。

结果

我们发现，催产素逆转LTP的Aβ引起的减值_{25 - 35}灌注在小鼠海马。这些作用被选择性催产素受体拮抗剂L-368,899阻断。此外，用ERK抑制剂U0126和选择性的Ca ²⁺可渗透的AMPA受体拮抗剂NASPM治疗完全拮抗了催产素的作用。

结论

这是第一个证明催产素可以逆转Aβ对小鼠海马LTP的影响的报道。我们建议ERK磷酸化和Ca 2 ⁺渗透性AMPA受体参与催产素的这种作用。