經顱性磁刺激TMS（Transcranial Magnetic Stimulation）是以非侵入性的方式來對大腦皮層神經元產生去極化或過極化。目前以廣泛的運用到許多神經退化性疾病上，例如帕金森氏症，肌張力不全症等。
在過去的研究中顯示，將TMS以burst的形式（Theta Burst Stimulation）施予刺激，對於改善肌張力不全病患的動作障礙有顯著效果，被認為可能的原因是TMS造成的長期突觸可塑性，使得病患受損的神經迴路能暫時性的恢復正常。有關這方面的理論模型並不多，因此，我們提出一個細胞層級的單一神經元模型，並且假設結合前突觸端的短期可塑性經由後突觸端的鈣離子濃度影響後突觸端的長期可塑性，模擬目前各種不同的TMS刺激方式所造成的突觸可塑性。
我們有相當好的模擬結果，與實驗結果相符以支持我們的假設。在各種不同的TMS刺激方式所造成的前突觸端的短期可塑性將會對後突觸端的長期可塑性產生決定性的影響。

Transcranial magnetic simulations (TMS) is an effective tool for studying pathophysiology of dystonia as well as various other movement or cognitive functions of the brain. In previous studies, synaptic plasticity induced by TMS might be the key of recovering the abnormality in motor cortex.
To study how TMS induces complex plasticity, we built computational models for pre-synaptic short-term plasticity and post-synaptic calcium dependent plasticity. With integration of these different time scale plasticity, Our model have successfully reproduced neural plasticity induced by a number of repetitive TMS protocols and Theta Burst stimulation (TBS).We will be able to provide insights into neuronal mechanisms underlying the effectiveness of TMS.
Our result indicates that pre-synaptic short-term plasticity affects post-synaptic long-term plasticity by changing calcium concentration.

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