ERK1/2 通过 L 型钙通道抑制突触囊泡胞吐。
Erk1/2 inhibit synaptic vesicle exocytosis through L-type calcium channels.
机构信息
Unit on Behavioral Genetics, Laboratory of Molecular Pathophysiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, USA.
出版信息
J Neurosci. 2011 Mar 23;31(12):4755-64. doi: 10.1523/JNEUROSCI.6594-10.2011.
Abstract
L-type calcium channels play only a minor role in basal neurotransmitter release in brain neurons but contribute significantly after induction of plasticity. Very little is known about mechanisms that enable L-type calcium channel participation in neurotransmitter release. Here, using mouse primary cortical neurons, we found that inhibition of Erk1/2 (extracellular signal-regulated kinases 1 and 2) enhanced synaptic vesicle exocytosis by increasing calcium influx through L-type calcium channels. Furthermore, inhibition of Erk1/2 increased the surface fraction of these channels. These findings indicate a novel inhibitory effect of Erk1/2 on synaptic transmission through L-type calcium channels.
摘要
L 型钙通道在大脑神经元的基础神经递质释放中仅发挥次要作用，但在诱导可塑性后贡献显著。关于使 L 型钙通道参与神经递质释放的机制知之甚少。在这里，我们使用小鼠原代皮质神经元发现，通过增加 L 型钙通道的钙内流来抑制 Erk1/2（细胞外信号调节激酶 1 和 2）可增强突触囊泡胞吐作用。此外，抑制 Erk1/2 增加了这些通道的表面分数。这些发现表明 Erk1/2 通过 L 型钙通道对突触传递具有新的抑制作用。
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