The molecular evidence of neural plasticity induced by cerebellar repetitive transcranial magnetic stimulation in the rat brain: A preliminary report

Cerebellar repetitive transcranial magnetic stimulation (rTMS) has been applied to treat several pathological conditions with insufficient evidence of molecular mechanism. Neural plasticity is proposed as one of mechanism. This study aimed to (1) confirm the feasibility of focal stimulation over cerebellar cortex and (2) investigate cerebellar rTMS effects on molecular changes associated with neural plasticity in the rat. For feasibility, six male Sprague-Dawley rats underwent ¹⁸F-FDG positron emission tomography (PET) to confirm focal stimulation on the cerebellar cortex after rTMS. For molecular evidence, thirty rats underwent a single (N=15) or 10 sessions (N=15) of rTMS with low-, high-frequency, or sham stimulation. In cerebellar cortex, reverse-transcriptase polymerase chain reaction and western blotting were performed on mRNA and proteins associated with neural plasticity: metabotrophic glutamate receptor 1 (GluR1), 2-amino-5-methyl-4-isoxazole-propionatic acid (AMPA) receptor (GluR2) and protein kinase C (PKC). As a result, ¹⁸F-FDG-PET showed an increase of glucose metabolism in the cerebellar cortex. The transcription of mGluR1 decreased following a single session of high-frequency rTMS. Synthesis of mGluR, PKC and GluR2 was reduced after rTMS, especially high frequency stimulation. It is suggested that rTMS could focus on the cerebellar cortex in the rat and induce neural plasticity associated with long-term depression.