One problem in motor control concerns the mechanism whereby the central nervous system translates the motor cortical command encoded in cell activity into a coordinated contraction of limb muscles to generate a desired motor output. This problem is closely related to the design of adaptive systems that transform neuronal signals chronically recorded from the motor cortex into the physiologically appropriate motor output of multijoint prosthetic limbs. In this study we demonstrated how this transformation can be carried out by an artificial neural network using as command signals the actual impulse activity obtained from recordings in the motor cortex of monkeys during the performance of a task that required the exertion of force in different directions. The network receives experimentally measured brain signals and recodes them into motor actions of a simulated actuator that mimics the primate arm. The actuator responds to the motor cortical commands with surprising fidelity, generating forces in close quantitative agreement with those exerted by trained monkeys, in both the temporal and spatial domains. Moreover, we show that the time-varying motor output may be controlled by the impulse activity of as few as 15 motor cortical cells. These results outline a potentially implementable computation scheme that utilizes raw neuronal signals to drive artificial mechanical systems.
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Sci Robot
January 2025
Sony Computer Science Laboratories Inc. (Sony CSL), Tokyo, Japan.
For trained individuals such as athletes and musicians, learning often plateaus after extensive training, known as the "ceiling effect." One bottleneck to overcome it is having no prior physical experience with the skill to be learned. Here, we challenge this issue by exposing expert pianists to fast and complex finger movements that cannot be performed voluntarily, using a hand exoskeleton robot that can move individual fingers quickly and independently.
View Article and Find Full Text PDFEur J Neurosci
January 2025
Department of Kinesiology, Trent University, Peterborough, ON, Canada.
Previous research on resting muscles has shown that inter-pulse interval (IPI) duration influences transcranial magnetic stimulation (TMS) responses, which can introduce serious confounding variables into investigations if not accounted for. However, it is far less clear how IPI influences TMS responses in active muscles. Thus, the purpose of this study was to examine the relationship between IPI and corticospinal excitability during submaximal isometric elbow flexion.
View Article and Find Full Text PDFNPJ Parkinsons Dis
January 2025
Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, 20852, USA.
ΑBSTRACT: In Parkinson's disease (PD), Lewy pathology deposits in the cerebral cortex, but how the pathology disrupts cortical circuit integrity and function remains poorly understood. To begin to address this question, we injected α-synuclein (αSyn) preformed fibrils (PFFs) into the dorsolateral striatum of mice to seed αSyn pathology in the cortical cortex and induce degeneration of midbrain dopaminergic neurons. We reported that αSyn aggregates accumulate in the motor cortex in a layer- and cell-subtype-specific pattern.
View Article and Find Full Text PDFJ Neural Eng
January 2025
Department of Neurology, Northwestern University Feinberg School of Medicine, 320 East Superior St, Chicago, IL 60611, USA, Chicago, Illinois, 60611, UNITED STATES.
Brain-machine interfaces (BMIs) have advanced greatly in decoding speech signals originating from the speech motor cortices. Primarily, these BMIs target individuals with intact speech motor cortices but who are paralyzed by disrupted connections between frontal cortices and their articulators due to brainstem stroke or motor neuron diseases such as amyotrophic lateral sclerosis. A few studies have shown some information outside the speech motor cortices, such as in parietal and temporal lobes, that also may be useful for BMIs.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Key Laboratory of Prevention and treatment of cardiovascular and cerebrovascular diseases of Ministry of Education, Gannan Medical University, Ganzhou, 341000, China.
Cerebral ischemia-induced pyroptosis contributes to the dissemination of neuroinflammation, and Nod-like receptor protein-3 (NLRP3) inflammasome plays a key role in this process. Previous studies have indicated that Genistein-3'-sodiumsulfonate (GSS) can inhibit neuroinflammation caused by cerebral ischemia, exert cerebroprotective effects, but its specific mechanism has not been comprehensively understood. The aim of this study was to explore the effect of GSS on ischemic stroke-induced cell pyroptosis.
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