Rap1 signaling prevents L-type calcium channel-dependent neurotransmitter release.
Rap1 signaling prevents L-type calcium channel-dependent neurotransmitter release.
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DOI：
10.1523/jneurosci.5963-11.2013
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发表时间：
2013-04-24
期刊：
影响因子：
--
通讯作者：
Morozov A
中科院分区：
文献类型：
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作者：
Subramanian J;Dye L;Morozov A
小的GTPase Rap1通过抑制皮质神经元的谷氨酸释放而促进恐惧学习和杏仁皮质的可塑性，但这种抑制的机制尚不清楚。另一方面，L型钙通道(LTCC)在恐惧学习和LTP诱导后参与谷氨酸释放。在这里，我们表明，在小鼠的初级皮质神经元中，Rap1的缺失增加了突触小泡的胞吐作用，而不改变内吞作用或囊泡池的大小，这是一种LTCC依赖的方式。我们确认ERK1/2是RAP1的下游效应因子，并表明它的抑制增加了突触前终末附近LTCC的质膜表达。我们认为，Rap1信号通过调节皮质-杏仁核突触的LTCC来实现可塑性和恐惧学习。
The small GTPase Rap1 contributes to fear learning and cortico-amygdala plasticity by inhibiting glutamate release from cortical neurons, but mechanisms of this inhibition remain unknown. On the other hand, L-type calcium channels (LTCC) become involved in glutamate release upon fear learning and LTP induction. Here, we show that Rap1 deletion in mouse primary cortical neurons increases synaptic vesicle exocytosis without altering endocytosis or vesicle pool size, in a LTCC dependent manner. We identify Erk1/2 as the downstream effector of Rap1 and show that its inhibition increases plasma membrane expression of LTCC near presynaptic terminals. We propose that the Rap1 signaling enables plasticity and fear learning by regulating LTCC at cortico-amygdala synapses.