scholarly journals Cerebellar GABA change during visuomotor adaptation relates to adaptation performance and cerebellar network connectivity: A Magnetic Resonance Spectroscopic Imaging study.

2021 ◽  
Author(s):  
Caroline R Nettekoven ◽  
Leah Mitchell ◽  
William T Clarke ◽  
Uzay Emir ◽  
Heidi Johansen-Berg ◽  
...  

Motor adaptation is crucial for performing accurate movements in a changing environment and relies on the cerebellum. Although cerebellar involvement has been well characterized, the neurochemical changes in the cerebellum that underpin human motor adaptation remain unknown. We used a novel Magnetic Resonance Spectroscopic Imaging (MRSI) technique to measure changes in the major inhibitory neurotransmitter γ-aminobutyric acid (GABA) in the human cerebellum during visuomotor adaptation. Participants used their right hand to adapt to a rotated cursor in the scanner, compared with a control task requiring no adaptation. We were able to spatially resolve adaptation-driven GABA changes at the cerebellar nuclei and in the cerebellar cortex in the left and the right cerebellar hemisphere independently and found that simple movement of the right hand increases GABA in the right cerebellar nuclei and decreases GABA in the left. When isolating adaptation-driven GABA changes, we found an increase in GABA in the left cerebellar nuclei and a decrease in GABA in the right cerebellar nuclei during adaptation. Early adaptation-driven GABA change in the right cerebellar nuclei correlated with adaptation performance: Participants showing greater GABA decrease adapted better, suggesting that this early GABA change is behaviourally relevant. Early GABA change also correlated with functional connectivity change in a cerebellar network: Participants showing a greater decrease in GABA also showed greater strength increase in cerebellar network connectivity. These results were specific to GABA, specific to adaptation and specific to the cerebellar network. This study provides the first evidence for plastic changes in cerebellar neurochemistry during a motor adaptation task. Characterising these naturally occurring neurochemical changes may provide a basis for developing therapeutic interventions to facilitate neurochemical changes in the cerebellum that can improve human motor adaptation.

NeuroImage ◽  
2012 ◽  
Vol 59 (1) ◽  
pp. 582-600 ◽  
Author(s):  
Robert A. Scheidt ◽  
Janice L. Zimbelman ◽  
Nicole M.G. Salowitz ◽  
Aaron J. Suminski ◽  
Kristine M. Mosier ◽  
...  

Author(s):  
Seung-Yeon Kim ◽  
Jae-Woon Kwon ◽  
Jin-Min Kim ◽  
Frank Chong-Woo Park ◽  
Sang-Hoon Yeo

Primitive-based models of motor learning suggest that adaptation occurs by tuning the responses of motor primitives. Based on this idea, we consider motor learning as an information encoding procedure, that is, a procedure of encoding a motor skill into primitives. The capacity of encoding is determined by the number of recruited primitives, which depends on how many primitives are "visited" by the movement, and this leads to a rather counter-intuitive prediction that faster movement, where a larger number of motor primitives are involved, allows learning more complicated motor skills. Here we provide a set of experimental results that support this hypothesis. First, we show that learning occurs only with movement, i.e., only with non-zero encoding capacity. When participants were asked to counteract a rotating force applied to a robotic handle, they were unable to do so when maintaining a static posture but were able to adapt when making small circular movements. Our second experiment further investigated how adaptation is affected by movement speed. When adapting to a simple (low-information-content) force field, fast (high-capacity) movement did not have an advantage over slow (low-capacity) movement. However, for a complex (high-information-content) force field, the fast movement showed a significant advantage over slow movement. Our final experiment confirmed that the observed benefit of high-speed movement is only weakly affected by mechanical factors. Taken together, our results suggest that the encoding capacity is a genuine limiting factor of human motor adaptation.


eNeuro ◽  
2020 ◽  
Vol 7 (1) ◽  
pp. ENEURO.0149-19.2019 ◽  
Author(s):  
Frédéric Crevecoeur ◽  
Jean-Louis Thonnard ◽  
Philippe Lefèvre

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Jan Babič ◽  
Erhan Oztop ◽  
Mitsuo Kawato

2019 ◽  
Vol 9 (5) ◽  
pp. 122 ◽  
Author(s):  
Kalyan Yarraguntla ◽  
Fen Bao ◽  
Samuel Lichtman-Mikol ◽  
Sara Razmjou ◽  
Carla Santiago-Martinez ◽  
...  

Few cross-sectional studies have investigated the correlation between neurochemical changes and multiple sclerosis (MS) fatigue, but little is known on the fatigue-related white matter differences between time points. We aim to investigate the longitudinal neurometabolite profile of white matter in MS fatigue. Forty-eight relapsing remitting multiple sclerosis (RRMS) patients with an expanded disability status scale (EDSS) ≤ 4 underwent high field 1H-multivoxel magnetic resonance spectroscopy (MRS) at baseline and year 1. Fatigue severity was evaluated by the fatigue severity scale (FSS). Patients were divided into low (LF, FSS ≤ 3), moderate (MF, FSS = 3.1–5), and high fatigue (HF, FSS ≥ 5.1) groups. In a two-way analysis of variance (ANOVA), we observed a decline in the ratio of the sum of N-acetylaspartate (NAA) and N-acetylaspartylglutamate (NAAG) to the sum of creatine (Cr) and phosphocreatine (PCr) in the right anterior quadrant (RAQ) and left anterior quadrant (LAQ) of the MRS grid in the HF group at baseline and year 1. This decline was significant when compared with the LF group (p = 0.018 and 0.020). In a one-way ANOVA, the fatigue group effect was significant and the ratio difference in the right posterior quadrant (RPQ) and left posterior quadrant (LPQ) of the HF group was also significant (p = 0.012 and 0.04). Neurochemical changes in the bilateral frontal white matter and possibly parietooccipital areas were noted in the HF group at two different time points. Our findings may shed some light on the pathology of MS fatigue.


Sign in / Sign up

Export Citation Format

Share Document