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首页> 外文期刊>Journal of Computational Neuroscience >Calcium control of triphasic hippocampal STDP
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Calcium control of triphasic hippocampal STDP

机译：钙离子控制海马STDP

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摘要

Synaptic plasticity is believed to represent the neural correlate of mammalian learning and memory func tion. It has been demonstrated that changes in synaptic conductance can be induced by approximately synchronous pairings of pre- and post- synaptic action potentials deliv ered at low frequencies. It has also been established that NMDAr-dependent calcium influx into dendritic spines rep resents a critical signal for plasticity induction, and can account for this spike-timing dependent plasticity (STDP) as well as experimental data obtained using other stimula tion protocols. However, subsequent empirical studies have delineated a more complex relationship between spike timing, firing rate, stimulus duration and post-synaptic bursting in dictating changes in the conductance of hippo campal excitatory synapses. Here, we present a detailed biophysical model of single dendritic spines on a CA1 pyramidal neuron, describe the NMDAr-dependent calcium influx generated by different stimulation protocols, and con struct a parsimonious model of calcium driven kinase and phosphatase dynamics that dictate the probability of stochastic transitions between binary synaptic weight states in a Markov model. We subsequently demonstrate that this approach can account for a range of empirical observations regarding the dynamics of synaptic plasticity induced by different stimulation protocols, under regimes of pharmaco logical blockade and metaplasticity. Finally, we highlight the strengths and weaknesses of this parsimonious, unified computational synaptic plasticity model, discuss differences between the properties of cortical and hippocampal plastic ity highlighted by the experimental literature, and the man ner in which further empirical and theoretical research might elucidate the cellular basis of mammalian learning and memory function.
机译：突触可塑性被认为代表了哺乳动物学习和记忆功能的神经相关性。已经证明，可以通过以低频分配的突触前和突触后动作电位的近似同步配对来诱导突触电导的变化。还已经确定，依赖NMDAr的钙流入树突棘代表了可塑性诱导的关键信号，并且可以解释这种依赖于尖峰时间的可塑性（STDP）以及使用其他刺激方案获得的实验数据。然而，随后的实证研究表明，尖峰时间，击发率，刺激持续时间和突触后爆发之间的更复杂关系决定了河马营地兴奋性突触电导的变化。在这里，我们介绍了CA1锥体神经元上的单个树突棘的详细的生物物理模型，描述了由不同刺激方案产生的依赖于NMDAr的钙内流，并构建了一个由钙驱动的激酶和磷酸酶动力学的简化模型，该模型决定了随机发生的可能性马尔可夫模型中二进制突触权重状态之间的转换。我们随后证明，该方法可解释一系列关于在药代动力学和药物代谢阻滞下由不同刺激方案诱导的突触可塑性动力学的经验观察。最后，我们强调了这种简约的统一计算突触可塑性模型的优缺点，讨论了实验文献强调的皮质和海马可塑性特性之间的差异，以及进一步的经验和理论研究可能阐明了细胞哺乳动物学习和记忆功能的基础。

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