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Impact of Dendritic Size and Dendritic Topology on Burst Firing in Pyramidal Cells

机译:树突尺寸和树突拓扑对金字塔细胞爆发的影响

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Neurons display a wide range of intrinsic firing patterns. A particularly relevant pattern for neuronal signaling and synaptic plasticity is burst firing, the generation of clusters of action potentials with short interspike intervals. Besides ion-channel composition, dendritic morphology appears to be an important factor modulating firing pattern. However, the underlying mechanisms are poorly understood, and the impact of morphology on burst firing remains insufficiently known. Dendritic morphology is not fixed but can undergo significant changes in many pathological conditions. Using computational models of neocortical pyramidal cells, we here show that not only the total length of the apical dendrite but also the topological structure of its branching pattern markedly influences inter- and intraburst spike intervals and even determines whether or not a cell exhibits burst firing. We found that there is only a range of dendritic sizes that supports burst firing, and that this range is modulated by dendritic topology. Either reducing or enlarging the dendritic tree, or merely modifying its topological structure without changing total dendritic length, can transform a cell's firing pattern from bursting to tonic firing. Interestingly, the results are largely independent of whether the cells are stimulated by current injection at the soma or by synapses distributed over the dendritic tree. By means of a novel measure called mean electrotonic path length, we show that the influence of dendritic morphology on burst firing is attributable to the effect both dendritic size and dendritic topology have, not on somatic input conductance, but on the average spatial extent of the dendritic tree and the spatiotemporal dynamics of the dendritic membrane potential. Our results suggest that alterations in size or topology of pyramidal cell morphology, such as observed in Alzheimer's disease, mental retardation, epilepsy, and chronic stress, could change neuronal burst firing and thus ultimately affect information processing and cognition.
机译:神经元显示各种内在烧制图案。用于神经元信号传导和突触可塑性的特别相关的模式是突发烧制,产生短间隔间隔的动作电位簇的产生。除离子通道组合物外,树突形态似乎是调制烧制模式的重要因素。然而,潜在的机制理解得很差,并且形态对爆发烧制的影响仍然是不够的。树突状形态不是固定的,但可以在许多病理条件下进行重大变化。利用新皮质锥体细胞的计算模型,我们这里不仅表明了顶端树突的总长度,而且还具有其分支模式的拓扑结构,显着影响沟道间隔和沟道间隔,甚至确定细胞是否表现出突发烧制。我们发现只有一系列支持突发射击的树突尺寸,并且该范围由树突拓扑进行调制。减少或扩大树突树,或者仅在不改变总树枝状长度的情况下改变其拓扑结构,可以将细胞的烧制模式从爆裂转变为滋补烧制。有趣的是,结果在很大程度上独立于细胞是否通过SOMA的当前注射或分布在树突树上的突触刺激。通过一种称为平均电态路径长度的新型措施,我们表明树突状形态对突发烧制的影响是由于树枝状大小和树突拓扑结构,而不是体细胞输入电导,而是在平均空间范围内树突树和树突膜电位的时空动态。我们的研究结果表明,在阿尔茨海默病的疾病,智力延迟,癫痫和慢性应激中观察到锥体细胞形态的大小或拓扑的变化可以改变神经元爆发射击,从而影响信息处理和认知。

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