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Abstract Previous research has suggested that short‐term immobilization of the arm may be a low‐cost, non‐invasive strategy to enhance the capacity for long‐term potentiation (LTP)‐like plasticity in primary motor cortex (M1). Short‐term immobilization reduces corticospinal excitability (CSE) in the contralateral M1, and interhemispheric inhibition (IHI) from ipsi‐ onto contralateral M1 is increased. However, it is unclear whether reduced CSE and increased IHI are associated with changes in intracortical inhibition, which has been shown to be important for regulating neuroplasticity in M1. The current study used transcranial magnetic stimulation to evaluate the effects of short‐term (6 h) arm immobilization on CSE, IHI, and intracortical inhibition measured bilaterally in 43 neurotypical young adults (23 immobilized). We replicated previous findings demonstrating that immobilization decreased CSE in, and increased IHI onto, the immobilized hemisphere, but a significant change in intracortical inhibition was not observed at the group level. Across individuals, decreased CSE was associated with a decreased short‐interval intracortical inhibition, an index of GABAA‐ergic inhibition, within the immobilized hemisphere only in the immobilization group. Previous research has demonstrated that decreases in GABAA‐ergic inhibition are necessary for the induction of LTP‐like plasticity in M1; therefore, decreased intracortical inhibition after short‐term arm immobilization may provide a novel mechanism to enhance the capacity for LTP‐like plasticity within M1 and may be a potential target for strategies to augment plasticity capacity to enhance motor learning in health and disease.

Sensory loss involves irreversible behavioral and neural changes. Paradigms of short-term limb immobilization mimic deprivation of proprioceptive inputs and motor commands, which occur after the loss of limb use. While several studies have shown that short-term immobilization induced motor control impairments, the origin of such modifications is an open question. A Fitts’ pointing task was conducted, and kinematic analyses were performed to assess whether the feedforward and/or feedback processes of motor control were impacted. The Fitts’ pointing task specifically required dealing with spatial and temporal aspects (speed-accuracy trade-off) to be as fast and as accurate as possible. Forty trials were performed on two consecutive days by Control and Immobilized participants who wore a splint on the right arm during this 24 h period. The immobilization modified the motor control in a way that the full spatiotemporal structure of the pointing movements differed: A global slowdown appeared. The acceleration and deceleration phases were both longer, suggesting that immobilization impacted both the early impulse phase based on sensorimotor expectations and the later online correction phase based on feedback use. First, the feedforward control may have been less efficient, probably because the internal model of the immobilized limb would have been incorrectly updated relative to internal and environmental constraints. Second, immobilized participants may have taken more time to correct their movements and precisely reach the target, as the processing of proprioceptive feedback might have been altered.

Sensory loss involves irreversible behavioral and neural changes. Paradigms of short-term limb immobilization mimic deprivation of proprioceptive inputs and motor commands, which occur after the loss of limb use. While several studies have shown that short-term immobilization induced motor control impairments, the origin of such modifications is an open question. A Fitts' pointing task was conducted, and kinematic analyses were performed to assess whether the feedforward and/or feedback processes of motor control were impacted. The Fitts' pointing task specifically required dealing with spatial and temporal aspects (speed-accuracy trade-off) to be as fast and as accurate as possible. Forty trials were performed on two consecutive days by Control and Immobilized participants who wore a splint on the right arm during this 24 h period. The immobilization modified the motor control in a way that the full spatiotemporal structure of the pointing movements differed: A global slowdown appeared. The acceleration and deceleration phases were both longer, suggesting that immobilization impacted both the early impulse phase based on sensorimotor expectations and the later online correction phase based on feedback use. First, the feedforward control may have been less efficient, probably because the internal model of the immobilized limb would have been incorrectly updated relative to internal and environmental constraints. Second, immobilized participants may have taken more time to correct their movements and precisely reach the target, as the processing of proprioceptive feedback might have been altered. [ABSTRACT FROM AUTHOR]

Prolonged limb immobilization deprives sensorimotor cortical areas of an important source of excitatory input, as well as of motor output. Previous work has described effects on motor excitability but it is unclear whether motor plasticity is also influenced. In two groups of eight healthy human subjects, the left hand was immobilized for 8 h to induce sensorimotor deprivation of the cortical representation of the abductor pollicis brevis muscle. We used transcranial magnetic stimulation protocols to evaluate motor excitability with motor-evoked potentials, input- output (IOcurve) and short-latency intracortical inhibition (SICI) recruitment curves, as well as long-term potentiation (LTP)/long-term depression (LTD)-like plasticity with paired-associative stimulation (PAS) of the median nerve and motor cortex using an interstimulus interval of 25 ms (PAS25) or 10 ms (PAS10), respectively, in two sessions at least 7 d apart (baseline and after immobilization). After immobilization, the slope of the IOcurve decreased, and SICI at lower conditioning pulse intensities was reduced. The LTP-like effects of PAS25 and the LTD-like effect of PAS10 were both significantly enhanced. The effects differed among individuals: the more IOslope decreased after immobilization, the greater the increase of PAS25 and the smaller the increase of PAS10 effects. We suggest that sensorimotor deprivation has two effects. It increases the sensitivity to remaining sensory inputs and therefore increases the effectiveness of both PAS protocols. In addition, it reduces neuronal excitability to an individually different level, as reflected in the reduced IOslope and leads to an interdependent modulation of synaptic plasticity as such as it shifts the threshold of LTP/LTD-like plasticity induction. [ABSTRACT FROM AUTHOR]

Abstract: Sensorimotor function is important for cognitive development; however, little experimental evidence exists to support this assumption. In this study we tested the hypothesis that altered cAMP response element binding (CREB) protein induction and activity-regulated cytoskeletal-associated gene (Arc) expression may underlie the suppression of hippocampal neurogenesis and memory impairment associated with early sensorimotor deprivation. Associated memory was evaluated in sensorimotor deprived (T) and sham operated (C) rats using a contextual fear-conditioning task. Hippocampal dentate gyrus (DG) neurogenesis was assessed by Brdu and NeuN labeling. Hippocampal DG CREB signaling was examined by measuring protein and mRNA levels of CREB and activity-regulated cytoskeletal-associated gene (Arc). Contextual freezing responses in the 1-day recall test were significantly lower in 25- and 35-day-old group T compared to C rats (P <0.01), indicating that hippocampal-dependent memory impairment was caused by early sensorimotor deprivation. Furthermore, group T rats exhibited significantly decreased CREB and Arc activation in the hippocampal DG at 25 and 35 days compared to in group C rats (P <0.01 for both). These changes may underlie decreased neurogenesis and impaired memory. No significant between groups differences were apparent in 45- and 60-day-old rats. These results suggest that early sensorimotor deprivation may alter CREB signaling, decrease Arc activation, suppress neurogenesis and ultimately impair memory. [Copyright &y& Elsevier]

Abstract: This study examined the effects of early palmar forepaw sensorimotor deprivation on learning and memory in rats. Sensorimotor deprivation was performed on 18-day-old male rats. Controls were sham operated. Studies were performed on rats aged 18, 25, 35, 45 and 60 days. Morris water maze testing was used to assess learning and memory. Long-term potentiation (LTP) was assessed by electrophysiological means in slices obtained from the hippocampal Schaffer collateral pathway. Nissl staining was performed to assess pyramidal cell number in hippocampal CA1 and CA3 regions. Hippocampal N-methyl-d-aspartate receptor 1 (NMDAR1) mRNA and protein levels were assessed. Learning and short-term memory were significantly depressed in 25 and 35 day old sensorimotor deprived rats (P <0.01). LTP was also significantly depressed in sensorimotor deprived rats at these ages, while hippocampal CA1 pyramidal cell counts were significantly decreased (P <0.05). CA3 cell numbers were significantly lower in 25-day-old sensorimotor deprived rats (P <0.05). Both NMDAR1 mRNA and protein levels were significantly lower in sensorimotor deprived rats aged 25 and 35 days (P <0.05). These findings indicate that palmar surface forepaw sensorimotor deprivation impairs subsequent learning and memory in young rats. Decreased hippocampal pyramidal cell numbers and altered NMDAR1 expression may underlie this impairment. [Copyright &y& Elsevier]

Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Limb amputation is characterized by complex and intermingled brain reorganization processes combining sensorimotor deprivation induced by the loss of the limb per se, and compensatory behaviors, such as the over-use of the intact or remaining limb. While a large body of evidence documents sensorimotor representation plasticity following arm amputation, less investigations have been performed to fully understand the use-dependent plasticity phenomenon and the role of behavioral compensation in brain reorganization. In this article, I will review the findings on sensorimotor plasticity after limb amputation, focusing on these two aspects: sensorimotor deprivation and adaptive patterns of limb usage, and describe the models that attempt to link these reorganizational processes with phantom limb pain. Two main models have been proposed: the maladaptive plasticity model which states that the reorganization of the adjacent cortical territories into the representation of the missing limb is proportional to phantom pain intensity, and the persistent representation model, which rather suggests that the intensity of residual brain activity associated with phantom hand movements scales with phantom limb pain intensity. I will finally illustrate how this fundamental research helps designing new therapeutic strategies for phantom plain relief., (Copyright © 2021 The Author. Published by Elsevier Masson SAS.. All rights reserved.)

We investigated the embodied nature of motor imagery processes through a recent use-dependent plasticity approach, a short-term limb immobilization paradigm. A splint placed on the participants' left-hand during a brief period of 24 h was used for immobilization. The immobilized participants performed two mental rotation tasks (a hand mental rotation task and a number mental rotation task) before (pre-test) and immediately after (post-test) the splint removal. The control group did not undergo the immobilization procedure. The main results showed an immobilization-induced effect on left-hand stimuli, resulting in a lack of task-repetition benefit. By contrast, accuracy was higher and response times were shorter for right-hand stimuli. No immobilization-induced effects appeared for number stimuli. These results revealed that the cognitive representation of hand movements can be modified by a brief period of sensorimotor deprivation, supporting the hypothesis of the embodied nature of motor simulation processes.

Recent evidence suggests that immobilization of the upper limb for 2-3 weeks induces changes in cortical thickness as well as motor performance. In constraint induced (CI) therapy, one of the most effective interventions for hemiplegia, the non-paretic arm is constrained to enforce the use of the paretic arm in the home setting. With the present study we aimed to explore whether non-paretic arm immobilization in CI therapy induces structural changes in the non-lesioned hemisphere, and how these changes are related to treatment benefit. 31 patients with chronic hemiparesis participated in CI therapy with (N = 14) and without (N = 17) constraint. Motor ability scores were acquired before and after treatment. Diffusion tensor imaging (DTI) data was obtained prior to treatment. Cortical thickness was measured with the Freesurfer software. In both groups cortical thickness in the contralesional primary somatosensory cortex increased and motor function improved with the intervention. However the cortical thickness change was not associated with the magnitude of motor function improvement. Moreover, the treatment effect and the cortical thickness change were not significantly different between the constraint and the non-constraint groups. There was no correlation between fractional anisotropy changes in the non-lesioned hemisphere and treatment outcome. CI therapy induced cortical thickness changes in contralesional sensorimotor regions, but this effect does not appear to be driven by the immobilization of the non-paretic arm, as indicated by the absence of differences between the constraint and the non-constraint groups. Our data does not suggest that the arm immobilization used in CI therapy is associated with noticeable cortical thinning.