Kaplan Michael P, Abel Ted
Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6018, USA.
CNS Spectr. 2003 Aug;8(8):597-610. doi: 10.1017/s1092852900018873.
Long-term memory is believed to depend on long-lasting changes in the strength of synaptic transmission known as synaptic plasticity. Understanding the molecular mechanisms of long-term synaptic plasticity is one of the principle goals of neuroscience. Among the most powerful tools being brought to bear on this question are genetically modified mice with changes in the expression or biological activity of genes thought to contribute to these processes. This article reviews how strains of mice with alterations in the cyclic adenosine monophosphate/protein kinase A/cyclic adenosine monophosphate-response element-binding protein signaling pathway have advanced our understanding of the biological basis of learning and memory.
长期记忆被认为依赖于突触传递强度的持久变化,即所谓的突触可塑性。理解长期突触可塑性的分子机制是神经科学的主要目标之一。用于解决这个问题的最有力工具之一是基因表达或生物活性发生改变的转基因小鼠,这些基因被认为与这些过程有关。本文综述了环磷酸腺苷/蛋白激酶A/环磷酸腺苷反应元件结合蛋白信号通路发生改变的小鼠品系如何增进了我们对学习和记忆生物学基础的理解。