Hiratani Naoki, Fukai Tomoki
Department of Complexity Science and Engineering, The University of Tokyo, Kashiwa, Chiba, Japan; Research Fellow of Japan Society for the Promotion of Science, Chiyoda, Tokyo, Japan; Lab for Neural Circuit Theory, RIKEN Brain Science Institute, Wako, Saitama, Japan.
Department of Complexity Science and Engineering, The University of Tokyo, Kashiwa, Chiba, Japan; Lab for Neural Circuit Theory, RIKEN Brain Science Institute, Wako, Saitama, Japan; Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Kawaguchi, Saitama, Japan.
PLoS One. 2014 Jul 9;9(7):e101535. doi: 10.1371/journal.pone.0101535. eCollection 2014.
Various hippocampal and neocortical synapses of mammalian brain show both short-term plasticity and long-term plasticity, which are considered to underlie learning and memory by the brain. According to Hebb's postulate, synaptic plasticity encodes memory traces of past experiences into cell assemblies in cortical circuits. However, it remains unclear how the various forms of long-term and short-term synaptic plasticity cooperatively create and reorganize such cell assemblies. Here, we investigate the mechanism in which the three forms of synaptic plasticity known in cortical circuits, i.e., spike-timing-dependent plasticity (STDP), short-term depression (STD) and homeostatic plasticity, cooperatively generate, retain and reorganize cell assemblies in a recurrent neuronal network model. We show that multiple cell assemblies generated by external stimuli can survive noisy spontaneous network activity for an adequate range of the strength of STD. Furthermore, our model predicts that a symmetric temporal window of STDP, such as observed in dopaminergic modulations on hippocampal neurons, is crucial for the retention and integration of multiple cell assemblies. These results may have implications for the understanding of cortical memory processes.
哺乳动物大脑的各种海马体和新皮质突触既表现出短期可塑性，也表现出长期可塑性，这被认为是大脑学习和记忆的基础。根据赫布假说，突触可塑性将过去经历的记忆痕迹编码到皮质回路中的细胞集合中。然而，目前尚不清楚各种形式的长期和短期突触可塑性如何协同创建和重组此类细胞集合。在这里，我们研究了皮质回路中已知的三种突触可塑性形式，即尖峰时间依赖性可塑性（STDP）、短期抑制（STD）和稳态可塑性，在循环神经网络模型中协同生成、保留和重组细胞集合的机制。我们表明，由外部刺激产生的多个细胞集合可以在适当强度的STD噪声自发网络活动中存活。此外，我们的模型预测，如在海马神经元的多巴胺能调制中观察到的，STDP的对称时间窗口对于多个细胞集合的保留和整合至关重要。这些结果可能对理解皮质记忆过程有启示意义。
