Role of multiple calcium and calcium-dependent conductances in regulation of hippocampal dentate granule cell excitability

Role of multiple calcium and calcium-dependent conductances in regulation of hippocampal dentate granule cell excitability
复制标题

DOI:
10.1023/a:1008801821784
复制
发表时间:
1999-05-01
影响因子:
1.2
通讯作者:
Holmes, WR
Holmes, WR
中科院分区:
医学4区
文献类型:
--
作者:
Aradi, I;Holmes, WR

文献摘要

被引文献

相似文献

我们已经构建了一个详细的模型,海马齿状颗粒(DG)细胞,包括九种不同的通道类型。选择通道密度和分布,以重现在正常溶液中和应用阻断剂时观察到的报告的生理反应。该模型被用来探讨每种通道类型的贡献,特别强调的机制,潜在的postspike事件的尖峰行为。树突远端的T型钙电流对去极化后电位的出现有重要作用,其作用受BK型钙依赖性钾通道激活的控制。共激活和相互作用的N-,和/或L-型钙和AHP电流存在于体细胞和近端树突状细胞区域的模型DG细胞在响应于持久的电流注入的适应性。该模型被用来预测通道密度的变化,可能会导致癫痫爆发性放电,并预测影响的缓冲能力的变化对射击行为。我们的结论是,聚集的空间分布的钙相关通道,在树突的存在下,缓慢延迟整流钾电流,和钙缓冲特性,一起,可能解释的电阻DG细胞的发展致痫性爆发放电。
We have constructed a detailed model of a hippocampal dentate granule (DG) cell that includes nine different channel types. Channel densities and distributions were chosen to reproduce reported physiological responses observed in normal solution and when blockers were applied. The model was used to explore the contribution of each channel type to spiking behavior with particular emphasis on the mechanisms underlying postspike events. T-type calcium current in more distal dendrites contributed prominently to the appearance of the depolarizing after-potential, and its effect was controlled by activation of BK-type calcium-dependent potassium channels. Co-activation and interaction of N-, and/or L-type calcium and AHP currents present in somatic and proximal dendritic regions contributed to the adaptive properties of the model DG cell in response to long-lasting current injection. The model was used to predict changes in channel densities that could lead to epileptogenic burst discharges and to predict the effect of altered buffering capacity on firing behavior. We conclude that the clustered spatial distributions of calcium related channels, the presence of slow delayed rectifier potassium currents in dendrites, and calcium buffering properties, together, might explain the resistance of DG cells to the development of epileptogenic burst discharges.