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首页> 美国卫生研究院文献>The Journal of Physiology >Activity-dependent depression of the spike after-depolarization generates long-lasting intrinsic plasticity in hippocampal CA3 pyramidal neurons
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Activity-dependent depression of the spike after-depolarization generates long-lasting intrinsic plasticity in hippocampal CA3 pyramidal neurons

机译：去极化后棘突的活动依赖性抑制在海马CA3锥体神经元中产生持久的固有可塑性

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Persistent plastic changes to the intrinsic excitability of neurons have substantial implications for computational processing within the CNS. We have identified and characterized a novel long-lasting form of intrinsic plasticity in hippocampal CA3 pyramidal cells. Although the patterns of action potential firing elicited in this cell population by depolarizing current injections exhibited considerable diversity, practically all cells produced an initial high frequency (>100 Hz) burst of two to five spikes. This burst involved conductances that were responsible for the prominent spike afterdepolarization of CA3 pyramids. Long-lasting changes in the firing behaviour of CA3 cells were produced by conditioning stimuli (CS) consisting of either periods of depolarization in voltage clamp or periods of short (2 or 4 spikes) high frequency (circa 100 Hz) burst firing at 5 or 10 Hz. CS-induced changes included substantial prolongation of the first inter-spike interval and increased spike jitter. Similar CS-induced changes were seen when the test stimulus used to elicit firing resembled a glutamatergic EPSC. In line with this, a long-lasting depression of the ADP was elicited by the same CS that altered firing patterns of CA3 cells. Conditioning-induced changes in both spiking patterns and ADP amplitude were blocked by buffering intracellular Ca2+ with BAPTA. Furthermore, the Kv7 channel blocker XE991, a cognitive enhancer, both enhanced the ADP and completely eliminated its conditioning-induced depression. These findings indicate that a persistent enhancement of Kv7 channels, following a transient increase in cytoplasmic Ca2+, results in a prolonged depression of the ADP in CA3 pyramidal neurones.
机译：神经元固有兴奋性的持续塑性变化对中枢神经系统内的计算处理具有实质性影响。我们已经确定并表征了海马CA3锥体细胞内在可塑性的新型持久形式。尽管通过去极化电流注入在该细胞群中引起的动作电位激发的模式显示出相当大的多样性，但实际上所有细胞都产生了一个初始的高频率（> 100 Hz）的二到五个尖峰脉冲。这种爆发涉及电导，是导致CA3金字塔去极化后显着尖峰的原因。 CA3细胞放电行为的长期变化是通过调节刺激（CS）产生的，该刺激包括电压钳中的去极化周期或短时（2或4个尖峰）高频（约100 Hz）的突发放电（5或5或5 Hz或以下） 10赫兹CS引起的变化包括第一次尖峰间隔的大幅延长和尖峰抖动的增加。当用于激发射击的测试刺激类似于谷氨酸能EPSC时，可以看到类似的CS诱导的变化。与此相符，相同的CS改变了CA3细胞的发射模式，引起ADP的长期降低。通过用BAPTA缓冲细胞内Ca 2 + 来阻止条件诱导的尖峰模式和ADP幅度变化。此外，Kv7通道阻滞剂XE991（一种认知增强剂）既增强了ADP，又完全消除了其条件性诱发的抑郁症。这些发现表明，在细胞质Ca 2 + 瞬时增加后，Kv7通道的持续增强导致CA3锥体神经元中ADP的持续降低。

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