Cholinergic-mediated IP3-ereceptor activation induces long-lasting synaptic enhancement in CA1 pyramidal neurons
Cholinergic-mediated IP3-ereceptor activation induces long-lasting synaptic enhancement in CA1 pyramidal neurons
复制标题
DOI：
10.1523/jneurosci.2723-07.2008
复制
发表时间：
2008-02-06
影响因子：
5.3
通讯作者：
Buno, Washington
中科院分区：
文献类型：
--
作者：
Fernandez de Sevilla, David;Nunez, Angel;Buno, Washington
胆碱能-谷氨酸能相互作用影响突触可塑性的形式，这种可塑性被认为是调节记忆和学习的。我们在体外测试了乙酰胆碱(ACh)在CA1锥体神经元顶端树突对Schaffer侧支的持久突触增强的诱导作用，并在体内通过刺激胆碱能传入神经元进行了测试。在体外，ACh通过在脊髓内插入AMPA受体而诱导了一种钙波和突触增强。这种突触增强需要M受体(MAChRs)的激活和1，4，5-三磷酸肌醇(IP3)敏感储存区的钙释放，这种突触增强对NMDA受体的阻断不敏感，也被IP3阻断所触发。激活体内胆碱能传入可引起类似的阿托品敏感的突触增强。我们描述了一种新的形式的突触增强(LTPIP3)，它是通过激活mAChRs在体外和体内诱导的。我们得出结论，从突触后内质网库释放的钙离子是诱导这种独特形式的长时间突触增强的关键事件。
Cholinergic-glutamatergic interactions influence forms of synaptic plasticity that are thought to mediate memory and learning. We tested in vitro the induction of long-lasting synaptic enhancement at Schaffer collaterals by acetylcholine (ACh) at the apical dendrite of CA1 pyramidal neurons and in vivo by stimulation of cholinergic afferents. In vitro ACh induced a Ca2+ wave and synaptic enhancement mediated by insertion of AMPA receptors in spines. Activation of muscarinic ACh receptors (mAChRs) and Ca2+ release from inositol 1,4,5-trisphosphate (IP3)-sensitive stores were required for this synaptic enhancement that was insensitive to blockade of NMDA receptors and also triggered by IP3 uncaging. Activation of cholinergic afferents in vivo induced an analogous atropine-sensitive synaptic enhancement. We describe a novel form of synaptic enhancement (LTPIP3) that is induced in vitro and in vivo by activation of mAChRs. We conclude that Ca2+ released from postsynaptic endoplasmic reticulum stores is the critical event in the induction of this unique form of long-lasting synaptic enhancement.