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首页> 外文期刊>The European Journal of Neuroscience >Stressor-related impairment of synaptic transmission in hippocampal slices from alpha-synuclein knockout mice.
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Stressor-related impairment of synaptic transmission in hippocampal slices from alpha-synuclein knockout mice.

机译：来自α-突触核蛋白敲除小鼠海马切片中与应激源相关的突触传递损伤。

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The role of alpha-synuclein (alpha-Syn) has recently received considerable attention because it seems to play a role in Parkinson's disease (PD). Missense mutations in the alpha-Syn gene were found in autosomal dominant PD and alpha-Syn was shown to be a major constituent of protein aggregates in sporadic PD and other synucleinopathies. Under normal conditions, alpha-Syn protein is found exclusively in synaptic terminals. However, the potential participation of alpha-synuclein in maintaining and regulating synaptic efficacy is unknown. We have investigated the excitatory synaptic modulation of alpha-synuclein in CA1 pyramidal neurons, using the in vitro hippocampal slice technique. The 4-aminopyridine-induced increase of both spontaneous excitatory postsynaptic current (EPSC) frequency and amplitude was significantly higher in alpha-Syn wild-type than knockout mice, whereas basal spontaneous EPSC frequency and amplitude was similar in both animals. As the spontaneous synaptic activity was abolished by tetrodotoxin, which indicates that it was a result of action potential-mediated transmitter release from presynaptic terminals, spontaneous EPSC changes observed in alpha-Syn knockout mice suggest that these animals present a modification of synaptic transmission with a presynaptic origin. Presynaptic depression of evoked EPSCs by hypoxia or adenosine was significantly larger in alpha-Syn knockout than in wild-type mice, further supporting the hypothesis of regulation of synaptic transmission by alpha-Syn. Together, these observations indicate that the loss of alpha-Syn reduces synaptic efficacy when the probability of transmitter release is modified. We conclude that alpha-Syn might have important actions on the maintenance of the functional integrity of synaptic transmission and its regulation in hippocampus.
机译：最近，α-突触核蛋白（α-Syn）的作用备受关注，因为它似乎在帕金森氏病（PD）中起作用。在常染色体显性遗传PD中发现了α-Syn基因的错义突变，并且α-Syn被证明是散发PD和其他突触核蛋白病中蛋白质聚集体的主要成分。在正常情况下，仅在突触末端发现α-Syn蛋白。然而，尚不清楚α-突触核蛋白在维持和调节突触效力中的潜在参与。我们使用体外海马切片技术研究了CA1锥体神经元中α-突触核蛋白的兴奋性突触调节。 α-Syn野生型中4-氨基吡啶诱导的自发性兴奋性突触后电流（EPSC）频率和振幅的增加均显着高于基因敲除小鼠，而两种动物中的基础自发性EPSC频率和振幅均相似。由于河豚毒素消除了自发的突触活性，这表明这是动作电位介导的递质从突触前末端释放的结果，在α-Syn基因敲除小鼠中观察到的自发EPSC变化表明，这些动物表现出突触传递的改变，并伴有突触传递。突触前的起源。 α-Syn基因敲除引起的缺氧或腺苷诱发的EPSC突触前抑制明显大于野生型小鼠，进一步支持了α-Syn调控突触传递的假说。总之，这些观察结果表明，当调节递质释放的可能性时，α-Syn的丧失会降低突触效力。我们得出结论，α-Syn可能对维持突触传递的功能完整性及其在海马中的调节具有重要作用。

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