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首页> 外文期刊>The European Journal of Neuroscience >Postnatal development of temporal integration, spike timing and spike threshold regulation by a dendrotoxin-sensitive K+ current in rat CA1 hippocampal cells
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Postnatal development of temporal integration, spike timing and spike threshold regulation by a dendrotoxin-sensitive K+ current in rat CA1 hippocampal cells

机译:产后大鼠CA1海马细胞中树突毒素敏感的K +电流对时间整合,峰时间和峰阈值的调节

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Spike timing and network synchronization are important for plasticity, development and maturation of brain circuits. Spike delays and timing can be strongly modulated by a low-threshold, slowly inactivating, voltage-gated potassium current called D-current (ID). ID can delay the onset of spiking, cause temporal integration of multiple inputs, and regulate spike threshold and network synchrony. Recent data indicate that ID can also undergo activity-dependent, homeostatic regulation. Therefore, we have studied the postnatal development of ID-dependent mechanisms in CA1 pyramidal cells in hippocampal slices from young rats (P7-27), using somatic whole-cell recordings. At P21-27, these neurons showed long spike delays and pronounced temporal integration in response to a series of brief depolarizing current pulses or a single long pulse, whereas younger cells (P7-20) showed shorter discharge delays and weak temporal integration, although the spike threshold became increasingly negative with maturation. Application of α-dendrotoxin (α-DTX), which blocks ID, reduced the spiking latency and temporal integration most strongly in mature cells, while shifting the spike threshold most strongly in a depolarizing direction in these cells. Voltage-clamp analysis revealed an α-DTX-sensitive outward current (ID) that increased in amplitude during development. In contrast to P21-23, ID in the youngest group (P7-9) showed smaller peri-threshold amplitude. This may explain why long discharge delays and robust temporal integration only appear later, 3 weeks postnatally. We conclude that ID properties and ID-dependent functions develop postnatally in rat CA1 pyramidal cells, and ID may modulate network activity and plasticity through its effects on synaptic integration, spike threshold, timing and synchrony. Spike timing and network synchronization are important for plasticity, development and maturation of brain circuits. Spike delays and timing can be strongly modulated by a low-threshold, slowly inactivating, voltage-gated K+ current called D-current (ID). We found that ID properties and ID-dependent functions develop postnatally in rat CA1 pyramidal cells, and ID may modulate network activity and plasticity through its effects on synaptic integration, spike threshold, timing and synchrony.
机译:峰值时间和网络同步对于大脑电路的可塑性,发展和成熟很重要。峰值延迟和时序可以通过称为D电流(ID)的低阈值,缓慢失活的电压门控钾电流来强烈调节。 ID可以延迟尖峰的发生,引起多个输入的时间积分,并调节尖峰阈值和网络同步。最近的数据表明,ID还可以进行与活动有关的稳态调节。因此,我们使用体细胞全细胞记录研究了幼鼠(P7-27)海马切片CA1锥体细胞中ID依赖机制的出生后发育。在P21-27时,这些神经元响应一系列短暂的去极化电流脉冲或单个长脉冲而显示出长的尖峰延迟和明显的时间整合,而较年轻的细胞(P7-20)显示出较短的放电延迟和较弱的时间整合,尽管随着成熟,峰值阈值变得越来越负。阻止ID的α-树突毒素(α-DTX)的应用在成熟细胞中最大程度地降低了尖峰潜伏期和时间整合,同时在这些细胞中将去极化阈值在去极化方向上变化最大。电压钳分析显示,α-DTX敏感的向外电流(ID)在显影过程中振幅增加。与P21-23相比,年龄最小的组(P7-9)的ID显示较小的阈值幅度。这可以解释为什么长时间的出院延迟和强大的时间整合只会在出生后3周出现。我们得出的结论是,ID属性和ID依赖性功能在大鼠CA1锥体细胞出生后发育,ID可能通过其对突触整合,突波阈值,时间和同步性的影响来调节网络活动和可塑性。峰值时间和网络同步对于大脑电路的可塑性,发展和成熟很重要。峰值延迟和时序可以通过称为D电流(ID)的低阈值,缓慢失活的电压门控K +电流来强烈调节。我们发现ID属性和ID依赖功能在大鼠CA1锥体细胞出生后发展,ID可能通过其对突触整合,突波阈值,时间和同步性的影响来调节网络活动和可塑性。

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