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Co-variation of ionic conductances supports phase maintenance in stomatogastric neurons

机译:离子电导的共变支持气孔胃神经元的相维持

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Neuronal networks produce reliable functional output throughout the lifespan of an animal despite ceaseless molecular turnover and a constantly changing environment. Central pattern generators, such as those of the crustacean stomatogastric ganglion (STG), are able to robustly maintain their functionality over a wide range of burst periods. Previous experimental work involving extracellular recordings of the pyloric pattern of the STG has demonstrated that as the burst period varies, the inter-neuronal delays are altered proportionally, resulting in burst phases that are roughly invariant. The question whether spike delays within bursts are also proportional to pyloric period has not been explored in detail. The mechanism by which the pyloric neurons accomplish phase maintenance is currently not obvious. Previous studies suggest that the co-regulation of certain ion channel properties may play a role in governing neuronal activity. Here, we observed in long-term recordings of the pyloric rhythm that spike delays can vary proportionally with burst period, so that spike phase is maintained. We then used a conductance-based model neuron to determine whether co-varying ionic membrane conductances results in neural output that emulates the experimentally observed phenomenon of spike phase maintenance. Next, we utilized a model neuron database to determine whether conductance correlations exist in model neuron populations with highly maintained spike phases. We found that co-varying certain conductances, including the sodium and transient calcium conductance pair, causes the model neuron to maintain a specific spike phase pattern. Results indicate a possible relationship between conductance co-regulation and phase maintenance in STG neurons.
机译:尽管分子的不断转换和环境的不断变化,神经网络在动物的整个生命周期中仍可产生可靠的功能输出。中央模式发生器,例如甲壳动物的胃胃神经节(STG)的发生器,能够在很宽的爆发周期内稳健地保持其功能。先前涉及STG幽门模式的细胞外记录的实验工作表明,随着猝发周期的变化,神经元间的延迟会成比例地改变,从而导致猝发阶段大致不变。尚未详细探讨突发内的尖峰延迟是否也与幽门周期成正比的问题。幽门神经元完成阶段维持的机制目前尚不清楚。先前的研究表明,某些离子通道特性的共同调节可能在控制神经元活动中发挥作用。在这里,我们在幽门节律的长期记录中观察到,尖峰延迟可以与猝发周期成比例地变化,因此可以保持尖峰相位。然后,我们使用基于电导的模型神经元来确定离子膜电导的共变是否会导致神经输出模拟实验观察到的尖峰相维持现象。接下来,我们利用模型神经元数据库来确定电导率相关性在具有高度维持的尖峰相位的模型神经元群体中是否存在。我们发现,改变某些电导,包括钠和瞬时钙电导对,会使模型神经元保持特定的尖峰相位模式。结果表明,STG神经元的电导共调节和相维持之间可能存在关系。

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