Loss of sensory input increases the intrinsic excitability of layer 5 pyramidal neurons in rat barrel cortex
Loss of sensory input increases the intrinsic excitability of layer 5 pyramidal neurons in rat barrel cortex
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DOI：
10.1113/jphysiol.2009.180943
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发表时间：
2009-11-01
影响因子：
5.5
通讯作者：
Stuart, Greg J.
中科院分区：
文献类型：
--
作者：
Breton, Jean-Didier;Stuart, Greg J.
皮层地图的发展是经验依赖性的，在不同的皮层层有不同的关键期。先前在啮齿动物桶状皮层的研究表明，感觉剥夺导致2/3层和4层突触传递和可塑性的变化。在这里，我们研究了感觉剥夺的影响，位于大鼠桶皮质的第5层锥体神经元的内在特性，同时使用体细胞和树突记录。感觉剥夺是通过剪掉鼻子一侧的所有胡须来实现的。感觉输入的损失并没有改变体细胞活性和静息膜特性，并没有影响树突状细胞动作电位（AP）的反向传播。相反，感觉剥夺导致第5层锥体神经元的百分比增加，表现出爆发性放电。这与高频AP序列期间产生树枝状钙峰的阈值降低有关。细胞贴附记录用于评估树突状HCN通道的性质和表达的变化。这些实验表明，感觉剥夺导致顶端树突远端区域HCN通道密度下降。为了评估HCN下调对感觉剥夺后观察到的树突兴奋性增加的贡献，我们研究了阻断HCN通道的影响。阻断HCN通道消除了对照和剥夺神经元之间树突钙电发生的差异。总之，这些观察结果表明，感觉丧失导致皮层第5层锥体神经元的树突兴奋性增加。此外，他们认为感觉剥夺后增加的树突钙电发生部分是通过下调树突HCN通道介导的。
Development of the cortical map is experience dependent, with different critical periods in different cortical layers. Previous work in rodent barrel cortex indicates that sensory deprivation leads to changes in synaptic transmission and plasticity in layer 2/3 and 4. Here, we studied the impact of sensory deprivation on the intrinsic properties of layer 5 pyramidal neurons located in rat barrel cortex using simultaneous somatic and dendritic recording. Sensory deprivation was achieved by clipping all the whiskers on one side of the snout. Loss of sensory input did not change somatic active and resting membrane properties, and did not influence dendritic action potential (AP) backpropagation. In contrast, sensory deprivation led to an increase in the percentage of layer 5 pyramidal neurons showing burst firing. This was associated with a reduction in the threshold for generation of dendritic calcium spikes during high-frequency AP trains. Cell-attached recordings were used to assess changes in the properties and expression of dendritic HCN channels. These experiments indicated that sensory deprivation caused a decrease in HCN channel density in distal regions of the apical dendrite. To assess the contribution of HCN down-regulation on the observed increase in dendritic excitability following sensory deprivation, we investigated the impact of blocking HCN channels. Block of HCN channels removed differences in dendritic calcium electrogenesis between control and deprived neurons. In conclusion, these observations indicate that sensory loss leads to increased dendritic excitability of cortical layer 5 pyramidal neurons. Furthermore, they suggest that increased dendritic calcium electrogenesis following sensory deprivation is mediated in part via down-regulation of dendritic HCN channels.