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Synergy between short-term and long-term plasticity explains direction-selectivity in visual cortex

机译:短期和长期可塑性之间的协同作用解释了视皮层的方向选择性

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In this study, we examine whether short-term plasticity (STP) mediates learning rules governing long-term synaptic plasticity (LTSP). More specifically, we examine how the initial vesicle release probability can mediate long-term changes in synaptic strength. Given the importance of calcium-dependent modulation of synaptic transmission, as well as the temporal information to cortical computation, we examine whether STP can set the initial condition in modulating network connectivity strength and stability via spike-timing-dependent plasticity (STDP). Taking as a starting point the well-established Tsodyks-Markram (TM) rule for STP, we implement a model of two interconnected units receiving a train of incoming spikes first mediated by a mechanism of presynaptic STP. Extending the TM model, we then implement a mechanism of postsynaptic LTSP. By treating the two mechanisms synergistically, we manipulate the initial vesicle release probability of presynaptic STP and find that this process modulates long-term depression-mediated weight convergence, thus mediating the activity of postsynaptic responses. Furthermore, we show that an interaction between STP and LTSP jointly mediate neocortical synapses in explaining direction selectivity. Overall, results suggest that calcium-dependent modulation of synaptic strength mediates important consequences of neocortical response properties.
机译:在这项研究中,我们检查了短期可塑性(STP)是否介导了控制长期突触可塑性(LTSP)的学习规则。更具体地说,我们研究了初始囊泡释放概率如何介导突触强度的长期变化。考虑到钙依赖性突触传递的调制的重要性,以及皮质计算的时间信息,我们研究了STP是否可以通过依赖于尖峰时序的可塑性(STDP)来设置调制网络连接强度和稳定性的初始条件。以建立良好的STP Tsodyks-Markram(TM)规则为起点,我们实现了两个相互连接的单元的模型,该单元接收一系列突触前STP机制介导的传入突波。扩展TM模型,然后我们实现突触后LTSP机制。通过协同处理这两种机制,我们操纵突触前STP的初始囊泡释放概率,并发现该过程调节了长期的抑郁症介导的体重收敛,从而介导了突触后反应的活性。此外,我们表明STP和LTSP之间的相互作用共同介导新皮层突触,以解释方向选择性。总体而言,结果表明,钙依赖的突触强度调节介导了新皮层反应特性的重要后果。

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