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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Small G Proteins Exhibit Pattern Sensitivity In Mapk Activation During The Induction Of Memory And Synaptic Facilitation In Aplysia
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Small G Proteins Exhibit Pattern Sensitivity In Mapk Activation During The Induction Of Memory And Synaptic Facilitation In Aplysia

机译：小G蛋白在海马诱导记忆和突触促进过程中的Mapk激活中表现出模式敏感性。

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摘要

Memory formation is highly sensitive to specific patterns of training, but the cellular and molecular mechanisms underlying pattern sensitivity are not well understood. We explored this general question by using Aplysia californica as a model system. We examined the regulation of MAPK (ERK1/2) activation by small G proteins in the CNS by using different patterns of analog stimuli that mimic different patterns of behavioral training for memory induction. We first cloned and characterized the Aplysia homologs of the small G proteins, Ras and Rap1 (ApRas and ApRap, respectively). We next examined changes in ApRas and ApRap activity that accompany MAPK activation. Last, by delivering recombinant ApRas and ApRap into the CNS, we directly manipulated their activity and examined the resultant MAPK activation. We found that MAPK activation induced by analog training depends on the combined activity of ApRas and ApRap, rather than the individual activity of either one alone. Also, ApRas and ApRap have a complex role in MAPK activation: they can act as activators or inhibitors, depending on the specific pattern of the training. The pattern-sensitive regulation of MAPK by interactive ApRas and ApRap activity that we have identified could contribute to the molecular routing of different downstream effects of spatially localized MAPK required for the induction of specific pattern-sensitive forms of synaptic facilitation and memory.
机译：记忆形成对训练的特定模式高度敏感，但是对模式敏感的基础的细胞和分子机制尚不清楚。我们通过使用加州ly作为模型系统探索了这个一般性问题。我们通过使用模拟刺激的不同模式的记忆诱导模拟模式的不同模式，检查了CNS中小G蛋白对MAPK（ERK1 / 2）激活的调节。我们首先克隆并表征了小G蛋白Ras和Rap1（分别为ApRas和ApRap）的Aplysia同源物。接下来，我们检查了伴随MAPK激活的ApRas和ApRap活性的变化。最后，通过将重组ApRas和ApRap递送到CNS中，我们直接操纵了它们的活性并检查了产生的MAPK激活。我们发现，由模拟训练诱导的MAPK激活取决于ApRas和ApRap的联合活性，而不是依赖于任一个的单独活性。同样，ApRas和ApRap在MAPK激活中具有复杂的作用：它们可以充当激活剂或抑制剂，具体取决于训练的具体模式。我们已经确定，通过相互作用的ApRas和ApRap活性对MAPK进行模式敏感调节，可能有助于诱导特定的模式敏感形式的突触促进和记忆所需的空间定位MAPK下游效应的分子路由。

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