PDF(Pubmed)
Abstract：
Static magnetic stimulation (SMS) is a form of non-invasive brain stimulation that alters neural activity and induces neural plasticity that outlasts the period of stimulation. This can modify corticospinal excitability or motor behaviours, suggesting that SMS may alter the intrinsic excitability of neurons. In mammalian neurons, the axon initial segment (AIS) is the site of action potential initiation and undergoes structural plasticity (changes in length and position from the soma) as a homeostatic mechanism to counteract chronic changes in neuronal activity. We investigated whether the chronic application of SMS (6 and 48 h, 0.5 T) induces structural AIS plasticity in postnatally derived primary cortical neurons. Following 6 h of SMS, we observed a shortening in mean AIS length compared to control, that persisted 24 h post stimulation. In contrast, 48 h of SMS induced an immediate distal shift that persisted 24 h post-stimulation. Pharmacological blockade of voltage gated L/T-type calcium channels during stimulation did not prevent SMS-induced AIS structural plasticity. Our findings provide the foundation to expand the use of chronic SMS as a non-invasive method to promote AIS plasticity.
摘要：
静态磁刺激（SMS）是一种非侵入性脑刺激形式，可改变神经活动并诱导神经可塑性，从而延长刺激期。这可以改变皮质脊髓的兴奋性或运动行为，这表明SMS可能会改变神经元的内在兴奋性。在哺乳动物神经元中，轴突初始段（AIS）是动作电位启动的部位，并经历结构可塑性（从体细胞的长度和位置变化），作为一种稳态机制，以抵消神经元活动的慢性变化。我们调查了SMS的慢性应用(6和48小时，0.5T）在出生后衍生的原代皮质神经元中诱导结构AIS可塑性。经过6小时的短信，与对照相比，我们观察到平均AIS长度缩短，在刺激后24小时持续存在。相比之下,SMS的48小时诱导了立即的远端移位，并在刺激后24小时持续存在。刺激期间电压门控L/T型钙通道的药理学阻断并不能阻止SMS诱导的AIS结构可塑性。我们的发现为扩大慢性SMS作为促进AIS可塑性的非侵入性方法的使用提供了基础。
