Journal of neurophysiology
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The influence of stance width on frontal plane postural dynamics and coordination in human bipedal stance was studied. We tested the hypothesis that when subjects adopt a narrow stance width, they will rely heavily on nonlinear control strategies and coordinated counter-phase upper and lower body motion to limit center-of-mass (CoM) deviations from upright; as stance increases, the use of these strategies will diminish. Freestanding frontal plane body sway was evoked through continuous pseudorandom rotations of the support surface on which subjects stood with various stimulus amplitudes. ⋯ Results show that the narrow stance postural system is nonlinear across stimulus amplitude in both EO and EC conditions, whereas the wide stance postural system is more linear. The nonlinearity in narrow stance is likely caused by an amplitude-dependent sensory reweighting mechanism. Finally, lower body and upper body sway were approximately in-phase at low frequencies (<1 Hz) and out-of-phase at high frequencies (>1 Hz) across all stance widths, and results were therefore inconsistent with the hypothesis that subjects made greater use of coordinated counter-phase upper and lower body motion in narrow compared with wide stance conditions.
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The recovery of voluntary quadrupedal locomotion after an incomplete spinal cord injury can involve different levels of the CNS, including the spinal locomotor circuitry. The latter conclusion was reached using a dual spinal lesion paradigm in which a low thoracic partial spinal lesion is followed, several weeks later, by a complete spinal transection (i.e., spinalization). In this dual spinal lesion paradigm, cats can express hindlimb walking 1 day after spinalization, a process that normally takes several weeks, suggesting that the locomotor circuitry within the lumbosacral spinal cord had been modified after the partial lesion. ⋯ When no further locomotor improvement was observed, cats were spinalized. After spinalization, the hindlimb locomotor pattern rapidly reappeared, but left/right asymmetries in swing/stance durations observed after the partial lesion could disappear or reverse. It is concluded that, after a partial spinal lesion, the hindlimb locomotor pattern was actively maintained by new dynamic interactions between spinal and supraspinal levels but also by intrinsic changes within the spinal cord.
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Bidirectional interactions between neurons and glial cells are crucial to the genesis of pathological pain. The mechanisms regulating these interactions and the role of this process in relaying synaptic input in the spinal dorsal horn remain to be established. We studied the role of glutamate transporters in the regulation of such interactions. ⋯ Glial-derived glutamate acted on extrasynaptic N-methyl-d-aspartate (NMDA) receptors mainly composed of NR2B receptors and generated SICs, which led to depolarization and action potential generation in superficial spinal dorsal horn neurons. Thus glutamate transporters regulate glutamatergic neuron-glia interactions at spinal sensory synapses. When glutamate uptake is impaired, glial cells function like excitatory interneurons-they are activated by peripheral synaptic input and release glutamate to activate postsynaptic neurons in spinal pain pathways.
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Clinical Trial
Deep brain stimulation alleviates parkinsonian bradykinesia by regularizing pallidal activity.
Deep brain stimulation (DBS) of the basal ganglia can alleviate the motor symptoms of Parkinson's disease although the therapeutic mechanisms are unclear. We hypothesize that DBS relieves symptoms by minimizing pathologically disordered neuronal activity in the basal ganglia. In human participants with parkinsonism and clinically effective deep brain leads, regular (i.e., periodic) high-frequency stimulation was replaced with irregular (i.e., aperiodic) stimulation at the same mean frequency (130 Hz). ⋯ Thus we show that clinically useful DBS alleviates motor symptoms by regularizing basal ganglia activity and thereby improving thalamic relay fidelity. This work demonstrates that high-frequency stimulation alone is insufficient to alleviate motor symptoms: DBS must be highly regular. Descriptive models of pathophysiology that ignore the fine temporal resolution of neuronal spiking in favor of average neural activity cannot explain the mechanisms of DBS-induced symptom alleviation.
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Although there is converging experimental and clinical evidences suggesting that mental training with motor imagery can improve motor performance, it is unclear how humans can learn movements through mental training despite the lack of sensory feedback from the body and the environment. In a first experiment, we measured the trial-by-trial decrease in durations of executed movements (physical training group) and mentally simulated movements (motor-imagery training group), by means of training on a multiple-target arm-pointing task requiring high accuracy and speed. Movement durations were significantly lower in posttest compared with pretest after both physical and motor-imagery training. ⋯ No such improvements were observed in the eye-movement training group. Our results suggest that the brain uses state estimation, provided by internal forward model predictions, to improve motor performance during mental training. Furthermore, our results suggest that mental practice can, at least in young healthy subjects and if given after a short bout of physical practice, be successfully substituted to physical practice to improve motor performance.