Most primary sensory neurons (PSNs) generate a slowly-activating inward current in response to membrane hyperpolarization (I_h) and express HCN1 along with additional isoforms coding for hyperpolarization-activated channels (HCN). Changes in HCN expression may affect the excitability and firing patterns of PSNs, but retinal and inner ear PSNs do not fire action potentials, suggesting HCN channel roles may extend beyond excitability and cell firing control. In patients taking I_h blockers, photopsia triggered in response to abrupt changes in luminance correlates with impaired visual signal processing via parallel rod and cone pathways. Furthermore, in a mouse model of inherited retinal degeneration, HCN blockers or Hcn1 genetic ablation may worsen photoreceptors' demise. PSN's use of HCN channels to adjust either their firing rate or process signals generated by sensory transduction in non-spiking PSNs indicates HCN1 channels as a versatile tool with a novel role in sensory processing beyond firing control.

大多数初级感觉神经元 (PSN) 响应膜超极化 (I _h ) 产生缓慢激活的内向电流，并表达HCN1以及编码超极化激活通道 (HCN) 的其他同种型。HCN 表达的变化可能会影响 PSN 的兴奋性和放电模式，但视网膜和内耳 PSN 不会触发动作电位，这表明 HCN 通道的作用可能超出兴奋性和细胞放电控制。在服用 I _h阻滞剂的患者中，响应于亮度的突然变化而触发的光视与通过平行视杆和视锥通路的视觉信号处理受损相关。此外，在遗传性视网膜变性的小鼠模型中，HCN 阻滞剂或Hcn1基因消融可能会加剧光感受器的死亡。PSN 使用 HCN 通道来调整其发射率或由非尖峰 PSN 中的感觉转导产生的过程信号表明 HCN1 通道是一种多功能工具，在发射控制之外的感觉处理中具有新的作用。