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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Dendritic HCN2 channels constrain glutamate-driven excitability in reticular thalamic neurons.
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Dendritic HCN2 channels constrain glutamate-driven excitability in reticular thalamic neurons.

机译：树突状HCN2通道限制网状丘脑神经元中谷氨酸驱动的兴奋性。

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摘要

Hyperpolarization activated cyclic nucleotide (HCN) gated channels conduct a current, I(h); how I(h) influences excitability and spike firing depends primarily on channel distribution in subcellular compartments. For example, dendritic expression of HCN1 normalizes somatic voltage responses and spike output in hippocampal and cortical neurons. We reported previously that HCN2 is predominantly expressed in dendritic spines in reticular thalamic nucleus (RTN) neurons, but the functional impact of such nonsomatic HCN2 expression remains unknown. We examined the role of HCN2 expression in regulating RTN excitability and GABAergic output from RTN to thalamocortical relay neurons using wild-type and HCN2 knock-out mice. Pharmacological blockade of I(h) significantly increased spike firing in RTN neurons and large spontaneous IPSC frequency in relay neurons; conversely, pharmacological enhancement of HCN channel function decreased spontaneous IPSC frequency. HCN2 deletion abolished I(h) in RTN neurons and significantly decreased sensitivity to 8-bromo-cAMP and lamotrigine. Recapitulating the effects of I(h) block, HCN2 deletion increased both temporal summation of EPSPs in RTN neurons as well as GABAergic output to postsynaptic relay neurons. The enhanced excitability of RTN neurons after I(h) block required activation of ionotropic glutamate receptors; consistent with this was the colocalization of HCN2 and glutamate receptor 4 subunit immunoreactivities in dendritic spines of RTN neurons. The results indicate that, in mouse RTN neurons, HCN2 is the primary functional isoform underlying I(h) and expression of HCN2 constrains excitatory synaptic integration.
机译：超极化激活的环状核苷酸（HCN）门控通道传导电流I（h）; I（h）如何影响兴奋性和尖峰发射主要取决于亚细胞区室中的通道分布。例如，HCN1的树突状表达使海马和皮质神经元的体细胞电压反应和峰值输出正常化。我们以前报道过，HCN2主要在网状丘脑核（RTN）神经元的树突棘中表达，但这种非体细胞HCN2表达的功能影响仍然未知。我们检查了HCN2表达在调节RTN兴奋性和使用野生型和HCN2敲除小鼠从RTN到丘脑皮层中继神经元的GABA能输出中的作用。对I（h）的药理学阻断作用显着增加了RTN神经元的尖峰放电和中继神经元的大自发IPSC频率;相反，HCN通道功能的药理学增强降低了自发IPSC频率。 HCN2删除废除了RTN神经元中的I（h），并显着降低了对8-溴-cAMP和拉莫三嗪的敏感性。概括I（h）阻滞的作用，HCN2缺失增加了RTN神经元中EPSP的瞬时总和以及突触后中继神经元的GABA能输出。 I（h）阻断后，RTN神经元的兴奋性增强，需要激活离子型谷氨酸受体。与此一致的是在RTN神经元的树突棘中HCN2和谷氨酸受体4亚基免疫反应性的共定位。结果表明，在小鼠RTN神经元中，HCN2是I（h）的主要功能亚型，HCN2的表达限制了兴奋性突触整合。

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