Abstract

Background Transcranial direct current stimulation (tDCS) is a non-invasive technique that modulates excitability of neurons in the motor cortex. In particular, anodal tDCS leads to cortical facilitation and overall increase in excitability ( Nitsche et al., 2000 ). Objective Although the effects of anodal tDCS on modulating motor cortex activation have been reported, there is little evidence of long term reduction of GABA concentration following anodal stimulation. Therefore, to characterize the duration of after effects of primary motor cortex (M1) excitability following anodal stimulation, we performed repeated magnetic resonance spectroscopy (MRS) measurements of GABA for 60 min after the stimulation. Materials and methods Thirty-two right-handed healthy volunteers were recruited in RWTH Aachen University. GABA-edited spectra were acquired using 3 T Siemens scanner from a volume of interest of 3 × 3 × 3 cm (27 mL) carefully placed on the hand motor area of the left primary motor cortex [ Fig. 1 ]. MEGA-PRESS J-editing ( Mescher et al., 1998 ), was used for GABA detection. Data processing and quantification of spectra was performed with TARQUIN ( Wilson et al., 2011 ). Results An ANOVA was performed on percentage of GABA concentrations with stimulation (sham vs. anodal) and measurement (12 measurements: 2 pre-stimulation and 10 post-stimulation measurements taken every 6 min) as between- and within-participants factors. The main effects of stimulation was not significant F(1, 30) = 1.157, p = .291. However, main effect of measurement was significant F(11, 330) = 2.378 p = .008. Remarkably, the interaction of stimulation x measurement was significant F(11, 330) = 2.249, p = .0128 [ Fig. 2 ]. GABA concentration decreased significantly in the anodal stimulation group at first (20th minute) post-stimulation measurement, and then stayed the same at measurements eighth, ninth and tenth ts (3) Discussion and conclusion Our results revealed a significant early drop of GABA concentration within 20 min following anodal stimulation and late drop of GABA after 66th minutes until the last post stimulation measurement (86th min). Early and late decrease in GABA could be due to a decrease of activity of glutamic acid decarboxylase (GAD) 67 and long term depression like plasticity, respectively. This technique may open a new field of application for long-lasting neuroplastic induction, especially in the rehabilitation of stroke patients.

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