Induction of motor associative plasticity in the posterior parietal cortex-primary motor network

Chi-Chao Chao, Anke Ninija Karabanov, Rainer Paine, Ana Carolina de Campos, Sahana N Kukke, Tianxia Wu, Han Wang, Mark Hallett, Chi-Chao Chao, Anke Ninija Karabanov, Rainer Paine, Ana Carolina de Campos, Sahana N Kukke, Tianxia Wu, Han Wang, Mark Hallett

Abstract

There is anatomical and functional connectivity between the primary motor cortex (M1) and posterior parietal cortex (PPC) that plays a role in sensorimotor integration. In this study, we applied corticocortical paired-associative stimuli to ipsilateral PPC and M1 (parietal ccPAS) in healthy right-handed subjects to test if this procedure could modulate M1 excitability and PPC-M1 connectivity. One hundred and eighty paired transcranial magnetic stimuli to the PPC and M1 at an interstimulus interval (ISI) of 8 ms were delivered at 0.2 Hz. We found that parietal ccPAS in the left hemisphere increased the excitability of conditioned left M1 assessed by motor evoked potentials (MEPs) and the input-output curve. Motor behavior assessed by the Purdue pegboard task was unchanged compared with controls. At baseline, conditioning stimuli over the left PPC potentiated MEPs from left M1 when ISI was 8 ms. This interaction significantly attenuated at 60 min after left parietal ccPAS. Additional experiments showed that parietal ccPAS induced plasticity was timing-dependent, was absent if ISI was 100 ms, and could also be seen in the right hemisphere. Our results suggest that parietal ccPAS can modulate M1 excitability and PPC-M1 connectivity and is a new approach to modify motor excitability and sensorimotor interaction.

Keywords: associative plasticity; corticocortical paired-associative stimulation; motor cortex; parietal motor connectivity; posterior parietal cortex.

Published by Oxford University Press 2013. This work is written by (a) US Government employee(s) and is in the public domain in the US.

Figures

Figure 1.
Figure 1.
Design of the parietal ccPAS study. The parietal ccPAS contained 180 pairs of TMS stimuli delivered at 0.2 Hz. In each pair of stimuli, the TMS stimulus at PPC was always 8 ms before the TMS stimulus at the ipsilateral M1. The coils we used for ccPAS are custom-made coils with the handle perpendicular to the plane of the coil. In this figure, the white square with a cross inside represents the handle. Pegboard task, rMT, MEP, and I/O curve were evaluated before (baseline), and 15, 60, 120 min and 24 h (P15, P60, P120, and P24H) after the parietal ccPAS.
Figure 2.
Figure 2.
Effects of left parietal ccPAS on MEPs of left M1HAND. MEPs by left M1 TMS were recorded from right FDI muscle and were averaged from all subjects. There was a significant effect of Time in the corresponding repeated-measures ANOVA; the post hoc analysis showed a significant increase in MEP amplitude at P60 relative to the baseline, indicating left parietal ccPAS enhanced the cortical excitability of left M1. *P < 0.05.
Figure 3.
Figure 3.
Effects of left parietal ccPAS on the I/O curve of left M1HAND. (A) The MEPs were recorded from the right FDI with the intensities of TMS at 80%, 90%, 100%, 110%, 120%, 130%, 150%, 160%, and 170% of rMT. The plots represent the mean MEP amplitude averaged from all 12 subjects at different time points. The MEP amplitudes as a function of the TMS intensity at P60 and P120 were significantly different from those at baseline. The post hoc analysis showed an increased MEP amplitude compared with baseline at intensities of 120%, 140%, 150%, 160%, and 170% rMT at P60 and at intensities of 130%, 140%, 150%, 160%, and 170% rMT at P120. (B) There was no difference in the I/O curve between the baseline and 24 h after ccPAS. *P < 0.05; #P < 0.05.
Figure 4.
Figure 4.
Effects of parietal ccPAS on the PPC–M1 interaction. The mean MEP amplitudes for all 3 ISI (4, 6, and 8 ms) are expressed as percentage of the unconditioned MEP amplitude (TS alone) at each time point. Repeated-measures ANOVA showed an effect of ISI only at baseline, and a significant potentiation of MEPs was noted at ISI of 8 ms. This facilitating the effect of PPC on the ipsilateral M1 faded gradually after PPC–M1 ccPAS. *P < 0.05. TS: test stimulus alone.
Figure 5.
Figure 5.
Effects of parietal ccPAS in the right hemisphere. (A) Parietal ccPAS was performed in the right hemisphere and the MEPs evoked from the right or left M1HAND were recorded from the contralateral FDI muscle. Repeated-measures ANOVA showed that Time had a trend of facilitatory effects on the MEPs from the conditioned right M1 (P = 0.065), but not the unconditioned left M1 (P = 0.414). (B) Effects of right parietal ccPAS on the I/O curve of the right M1HAND. The MEP amplitudes as a function of the TMS intensity at P60 and P120 were significantly higher than those at baseline. *P < 0.05.

Source: PubMed

3
구독하다