轴突电压门控钾通道在 tDCS 中的作用。

The role of axonal voltage-gated potassium channels in tDCS.

机构信息

Sagol Department of Neurobiology, University of Haifa, Haifa, Israel.

出版信息

Brain Stimul. 2022 May-Jun;15(3):861-869. doi: 10.1016/j.brs.2022.05.019. Epub 2022 May 29.

DOI:10.1016/j.brs.2022.05.019

PMID:35640845

Abstract

BACKGROUND

Transcranial direct current stimulation (tDCS) is a non-invasive sub-threshold stimulation, widely accepted for its amelioration of distinct neuropsychiatric disorders. The weak electric field of tDCS modulates the activity of cortical neurons, which in turn modifies brain functioning. However, the underlying mechanisms for that are not fully understood.

OBJECTIVE/HYPOTHESIS: Previous studies demonstrated that the axons are the most sensitive subcellular compartment for tDCS-induced polarization. Moreover, it was posited that DCS-induced axonal polarization is amplified by modifying the conductance of ionic channels. We posit that voltage-gated potassium-channels that are highly expressed in axons play a crucial role in DCS-induced modulation of cortical neurons functioning.

METHODS

We examined the involvement of voltage-gated potassium-channels in the active modulation of spontaneous vesicle release by DCS. For that, we measured spontaneous excitatory postsynaptic currents (sEPSCs) from layer-V motor cortex during DCS application, while co-applying distinct voltage-gated potassium-channels blockers. Moreover, we examined the role of Kv1 potassium channels in DCS-induced modulation of action potential waveform at axon terminals by recording action potentials at terminal axon blebs during DCS application while locally inhibiting the Kv1 potassium-channels.

RESULTS

We demonstrated that inhibiting voltage-gated potassium-channels occluded the DCS-induced modulation of subthreshold presynaptic vesicle release. Moreover, we showed that inhibiting Kv1 voltage-gated potassium-channels also occluded the DCS-induced modulation of action potential waveform at axon terminals.

CONCLUSION

We suggest that DCS-induced depolarization inactivates the Kv1 potassium channels thus reducing potassium conductance, which amplifies axonal depolarization, subsequently enhancing the presynaptic component of synaptic transmission. Whereas DCS-induced hyperpolarization induces opposite effects.

摘要

背景

经颅直流电刺激（tDCS）是一种非侵入性亚阈刺激，因其改善多种神经精神疾病而被广泛接受。tDCS 的弱电场调节皮质神经元的活动，进而调节大脑功能。然而，其潜在机制尚未完全理解。

目的/假设：先前的研究表明，轴突是 tDCS 诱导极化中最敏感的亚细胞区室。此外，有人假设，DCS 诱导的轴突极化通过改变离子通道的电导来放大。我们假设在轴突中高度表达的电压门控钾通道在 DCS 诱导的皮质神经元功能调节中发挥关键作用。

方法

我们研究了电压门控钾通道在 DCS 诱导的自发囊泡释放的主动调节中的作用。为此，我们在 DCS 应用期间测量了 V 层运动皮层中的自发兴奋性突触后电流（sEPSC），同时共同应用了不同的电压门控钾通道阻滞剂。此外，我们通过在 DCS 应用期间记录末梢轴突小球上的动作电位，同时局部抑制 Kv1 钾通道，研究了 Kv1 钾通道在 DCS 诱导的动作电位波形调制中的作用。