Deep brain stimulation (DBS) in thalamic reticular nucleus (TRN) neuron provides a novel treatment for drug-resistant epilepsy via the induced electrical field (EFs). However, the mechanisms underlying EF effects remain unclear. This paper investigated how EFs regulate low-threshold dendritic Ca²⁺ (dCa) response and thus contribute to the input–output relationship of TRN cell. Our results showed that EFs modulate firing modes differently in a neuronal state-dependent manner. At the depolarized state, EFs only regulate the spike timing of a somatic stimulus-evoked single action potential (AP) with less contribution in the regulation of dCa response but could induce the transition between a dendritic stimulus-evoked single AP and a tonic burst of APs via the moderate regulation of dCa response. At the hyperpolarized state, EFs have significant effects on the dCa response, which modulate the large dCa response-dependent burst discharge and even cause a transition from this type of burst discharge to a single AP with less dCa response. Moreover, EF effects on stimulation threshold of somatic spiking prominently depend on EF-regulated dCa responses and the onset time differences between the stimulus and EF give rise to the distinct effect in the EF regulation of dCa responses. Finally, the larger neuronal axial resistance tends to result in the dendritic stimulus-evoked dCa response independent of somatic state. Interestingly, in this case, the EF application could reproduce the similar somatic state-dependent dCa response to dendritic stimulus which occurs in the case of lower axial resistance. These results suggest that the influence of EF on neuronal activities depends on neuronal intrinsic properties, which provides insight into understanding how DBS in TRN neuron modulates epilepsy from the point of view of biophysics.

丘脑网状核 （TRN） 神经元中的深部脑刺激 （DBS） 通过感应电场 （EF） 为耐药性癫痫提供了一种新的治疗方法。然而，EF 效应的潜在机制仍不清楚。本文研究了 EFs 如何调节低阈值树突状 Ca²⁺ （dCa） 反应，从而促进 TRN 细胞的输入-输出关系。我们的结果表明，EFs 以神经元状态依赖性方式以不同的方式调节放电模式。在去极化状态下，EF 仅调节体细胞刺激诱发的单动作电位 （AP） 的尖峰时间，对 dCa 反应的调节贡献较小，但可以通过 dCa 反应的适度调节诱导树突刺激诱发的单个 AP 和 AP 的强直爆发之间的过渡。在超极化状态下，EF 对 dCa 响应有显著影响，这会调节大的 dCa 响应依赖性突发放电，甚至导致从这种类型的突发放电过渡到 dCa 响应较少的单个 AP。此外，EF 对体细胞刺激阈值的影响显着取决于 EF 调节的 dCa 反应，刺激和 EF 之间的起效时间差异在 EF 调节 dCa 反应中产生明显的影响。最后，较大的神经元轴向阻力往往导致树突状刺激诱发的 dCa 反应，与躯体状态无关。有趣的是，在这种情况下，EF 应用程序可以重现在轴向阻力较低的情况下发生的类似的躯体状态依赖性 dCa 对树突刺激的响应。 这些结果表明，EF 对神经元活动的影响取决于神经元的内在特性，这为从生物物理学的角度理解 TRN 神经元中的 DBS 如何调节癫痫提供了见解。