Control of voluntary limb movement is predominantly attributed to the contralateral motor cortex. However, increasing evidence suggests the involvement of ipsilateral cortical networks in this process, especially in motor tasks requiring bilateral coordination, such as locomotion. In this study, we combined a unilateral thoracic spinal cord injury (SCI) with a cortical neuroprosthetic approach to investigate the functional role of the ipsilateral motor cortex in rat movement through spared contralesional pathways. Our findings reveal that in all SCI rats, stimulation of the ipsilesional motor cortex promoted a bilateral synergy. This synergy involved the elevation of the contralateral foot along with ipsilateral hindlimb extension. Additionally, in two out of seven animals, stimulation of a sub-region of the hindlimb motor cortex modulated ipsilateral hindlimb flexion. Importantly, ipsilateral cortical stimulation delivered after SCI immediately alleviated multiple locomotor and postural deficits, and this effect persisted after ablation of the homologous motor cortex. These results provide strong evidence of a causal link between cortical activation and precise ipsilateral control of hindlimb movement. This study has significant implications for the development of future neuroprosthetic technology and our understanding of motor control in the context of SCI.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11588340 | PMC |
http://dx.doi.org/10.7554/eLife.92940 | DOI Listing |
Brain Res
December 2024
Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Chronic traumatic encephalopathy (CTE) has attracted attention due to sports-related head trauma or repetitive mild traumatic brain injury (mTBI). However, the pathology of CTE remains underexplored. Reproducible and quantitative model of CTE has yet to be established.
View Article and Find Full Text PDFNeuroimage
December 2024
Department of Neurosurgery, Affiliated Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address:
Background: Parkinson's disease (PD) is a movement disorder caused by dopaminergic neurodegeneration. Both Levodopa (L-dopa) and Subthalamic Deep Brain Stimulation (STN-DBS) effectively alleviate symptoms, yet their cerebral effects remain under-explored. Understanding these effects is essential for optimizing treatment strategies and assessing disease severity.
View Article and Find Full Text PDFBrain Commun
December 2024
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94304, USA.
Co-pathology is frequent in Lewy body disease, which includes clinical diagnoses of both Parkinson's disease and dementia with Lewy bodies. Measuring concomitant pathology can improve clinical and research diagnoses and prediction of cognitive trajectories. Tau PET imaging may serve a dual role in Lewy body disease by measuring cortical tau aggregation as well as assessing dopaminergic loss attributed to binding to neuromelanin within substantia nigra.
View Article and Find Full Text PDFCommun Biol
December 2024
Department of Physiology and Pharmacology, Sapienza University, Rome, Italy.
Transitive inference allows people to infer new relations between previously experienced premises. It has been hypothesized that this logical thinking relies on a mental schema that spatially organizes elements, facilitating inferential insights. However, recent evidence challenges the need for these complex cognitive processes.
View Article and Find Full Text PDFJ Clin Invest
December 2024
Department of Neurology, UCSF, San Francisco, United States of America.
NMDA receptor mediated autoimmune encephalitis (NMDAR-AE) frequently results in persistent sensory-motor deficits, especially in children, yet the underlying mechanisms remain unclear. This study investigated the long- term effects of exposure to a patient-derived GluN1-specific monoclonal antibody (mAb) during a critical developmental period (from postnatal day 3 to day 12) in mice. We observed long-lasting sensory-motor deficits characteristic of NMDAR-AE, along with permanent changes in callosal axons within the primary somatosensory cortex (S1) in adulthood, including increased terminal branch complexity.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!