Abstract
Repetitive magnetic stimulation (rTMS), including theta burst stimulation (TBS), is capable of modulating motor cortical excitability through plasticity-like mechanisms and might have therapeutic potential for Parkinson's disease (PD). An animal model would be helpful for elucidating the mechanism of rTMS that remain unclear and controversial. Here, we have established a TMS model in rat and applied this model to study the impact of substantia nigra dopamine neuron on TBS-induced motor plasticity in PD rats. In parallel with human results, continuous TBS (cTBS) successfully suppressed motor evoked potentials (MEPs), while MEPs increased after intermittent TBS (iTBS) in healthy rats. We then tested the effect of iTBS in early and advanced 6-hydroxydopamine (6-OHDA)-lesioned PD. Moreover, dopaminergic neurons in substantia nigra and rotation behavior were assessed to correlate with the amount of iTBS-induced plasticity. In results, iTBS-induced potentiation was reduced in early PD rats and was absent in advanced PD rats. Such reduction in plasticity strongly correlated with the dopaminergic cell loss and the count of rotation in PD rats. In conclusion, we have established a TMS PD rat model. With the help of this model, we confirmed the loss of domaninergic neurons in substantia nigra resulting in reduced rTMS-induced motor plasticity in PD.
Highlights
Repetitive transcranial magnetic stimulation is capable of producing long-lasting changes of cortical excitability beyond the short period of stimulation
Following one-way analysis of variance (ANOVA) showed that motor evoked potentials (MEPs) were enhanced by intermittent TBS (iTBS) (F7,64 = 3.619, P = 0.002 in left limb and F7,64 = 2.60, P = 0.02 in right limb), whereas they were suppressed by continuous TBS (cTBS) (F7,64 = 2.51, P = 0.02 in left limb and F7,64 = 2.64, P = 0.02 in right limb)
We have set up an animal model for testing Repetitive transcranial magnetic stimulation (rTMS)-induced motor plasticity in vivo in rats
Summary
Repetitive transcranial magnetic stimulation (rTMS) is capable of producing long-lasting changes of cortical excitability beyond the short period of stimulation. RTMS protocols have been translated to use in animal models for understanding their mechanistic insights (Aydin-Abidin et al 2008; Benali et al 2011; Funke and Benali 2011; Ghiglieri et al 2012; Hoppenrath and Funke 2013; Volz et al 2013). Most of these studies focused on the mechanism at the cellular level. The physiological response to rTMS as measured in humans, for example, changes in motor evoked potentials (MEPs), has rarely been tested in the animal models. The literature is scant in the use of disease animal models for studying the plasticity phenomena of rTMS in disease conditions, which may provide insights into the underlying pathophysiology of the disease for future diagnostic purposes and therapeutic applications targeting synaptic plasticity
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