Rab3A is essential for mossy fibre long-term potentiation in the hippocampus
Rab3A is essential for mossy fibre long-term potentiation in the hippocampus
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DOI：
10.1038/41574
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发表时间：
1997-08-07
期刊：
影响因子：
64.8
通讯作者：
Nicoll, RA
中科院分区：
文献类型：
--
作者：
Castillo, PE;Janz, R;Nicoll, RA
中枢神经系统兴奋性突触的重复激活导致突触传递的长期增加，称为长时程增强(LTP)。人们普遍认为，这种突触可塑性可能是某些形式的学习和记忆的基础。LTP在大多数突触中涉及N-甲基-D-天冬氨酸(NMDA)亚型谷氨酸受体的激活，但在海马团纤维突触中的LTP不依赖于NMDA受体，并且有一个在突触前诱导和表达的成分(1)。它似乎是由突触前Ca~(2+)升高触发的(参考文献2，3)，需要蛋白激酶A(4-6)的激活，从而导致谷氨酸(3，7-10)的释放增加。有关递质(11-13)囊泡释放的生化步骤已知很多，但这些步骤都没有直接与长期突触可塑性有关。在这里，我们表明，尽管各种短期可塑性是正常的，在缺乏突触囊泡蛋白Rab3A的小鼠中，杂乱纤维突触的LTP被取消。
Repetitive activation of excitatory synapses in the central nervous system results in a long-lasting increase in synaptic transmission called long-term potentiation (LTP). It is generally believed that this synaptic plasticity may underlie certain forms of learning and memory. LTP at most synapses involves the activation of the NMDA (N-methyl-D-aspartate) subtype of glutamate receptor, but LTP at hippocampal messy fibre synapses is independent of NMDA receptors and has a component that is induced and expressed presynaptically(1). It appears to be triggered by a rise in presynaptic Ca2+ (refs 2, 3), and requires the activation of protein kinase A(4-6), which leads to an increased release of glutamate(3,7-10). A great deal is known about the biochemical steps involved in the vesicular release of transmitter(11-13), but none of these steps has been directly implicated in long-term synaptic plasticity. Here we show that, although a variety of short-term plasticities are normal, LTP at messy fibre synapses is abolished in mice lacking the synaptic vesicle protein Rab3A.