Neurexin-neuroligin transsynaptic interaction mediates learning-related synaptic remodeling and long-term facilitation in aplysia.
Neurexin-neuroligin transsynaptic interaction mediates learning-related synaptic remodeling and long-term facilitation in aplysia.
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DOI：
10.1016/j.neuron.2011.03.020
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发表时间：
2011-05-12
期刊：
影响因子：
16.2
通讯作者：
Kandel ER
中科院分区：
文献类型：
--
作者：
Choi YB;Li HL;Kassabov SR;Jin I;Puthanveettil SV;Karl KA;Lu Y;Kim JH;Bailey CH;Kandel ER
在突触处彼此发生异嗜性相互作用的Neurexin和neuroligin在一些自闭症谱系障碍患者中发生突变，自闭症谱系障碍是一组以社交和情感学习缺陷为特征的疾病。我们已经探索了neurexin和neuroligin在感觉-运动神经元突触的鳃退缩反射在Africsia经历敏化，一种简单的形式学习恐惧。我们发现，耗尽neurexin在突触前感觉神经元或neuroligin在突触后运动神经元废除长期促进和相关的突触前生长诱导的重复脉冲的5-羟色胺。此外，将与自闭症谱系障碍相关的神经连接素-3的R451 C突变引入运动神经元，可阻断中期和长期易化。我们的研究结果表明，neurexin-neuroligin相互作用的活动依赖性调节可能会控制长期记忆存储所需的跨突触信号传导，包括自闭症谱系障碍可能受损的情感记忆。
Neurexin and neuroligin, which undergo heterophilic interactions with each other at the synapse, are mutated in some patients with autism spectrum disorder, a set of disorders characterized by deficits in social and emotional learning. We have explored the role of neurexin and neuroligin at sensory-to-motor neuron synapses of the gill-withdrawal reflex in Aplysia that undergoes sensitization, a simple form of learned fear. We find that depleting neurexin in the presynaptic sensory neuron or neuroligin in the postsynaptic motor neuron abolishes both long-term facilitation and the associated presynaptic growth induced by repeated pulses of serotonin. Moreover, introduction into the motor neuron of the R451C mutation of neuroligin-3 linked to autism spectrum disorder blocks both intermediate-term and long-term facilitation. Our results suggest that activity-dependent regulation of the neurexin-neuroligin interaction may govern trans-synaptic signaling required for the storage of long-term memory, including emotional memory that may be impaired in autism spectrum disorder.
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DOI：
10.1073/pnas.1004433107
发表时间：
2010-06-29
影响因子：
11.1
作者：
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影响因子：
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影响因子：
64.5
作者：
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通讯作者：
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影响因子：
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作者：
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