Electrical stimulation to repair spinal cord injury
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PROVIDER: PRJNA989738 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the mechanism of electrical stimulation in the repair of spinal cord injury, we established a rat model of spinal cord injury. Then, we used RNA-SEQ data obtained from ES treatment and 6 different rat models of spinal cord injury for gene expression profile analysis.
2023-07-01 | GSE214291 | GEO
Project description:Electrical stimulation can augment or modify neuronal function and can have therapeutic benefits for certain neurological disorders. There is evidence that enhancing spinal excitability with either epidural or transcutaneous stimulation can restore some volitional motor output after spinal cord injury (SCI). Lumbosacral epidural stimulation temporarily improves locomotor and autonomic function in both rodents and humans with SCI. When combined with overground locomotor training enabled by a weight-supporting device, epidural electrical stimulation (EES) promotes extensive reorganization of residual neural pathways that improves locomotion after stopping stimulation. However, the exact mechanism underlying the reconstruction of spinal cord neural circuits with electrical stimulation is not yet known. Thus, we developed a epidural electrical and muscle stimulation(EEMS) system at the interface of the spinal cord and muscle to mimic feedforward and feedback electrical signals in spinal sensorimotor circuits. Using methods of motor function evaluation, neural circuit tracing and neural signal recording, we discovered a unique stimulus frequency of 10-20 Hz under EEMS conditions that was required for structural and functional reconstruction of spinal sensorimotor circuits. Single-cell transcriptome analysis of EEMS activated motoneurons characterized molecular networks involved in spinal sensorimotor circuit reconstruction. This study provides insights into neural signal decoding during spinal sensorimotor circuit reconstruction, and indicates a technological approach for the clinical treatment of SCI.
2023-12-05 | GSE243038 | GEO
Project description:Spinal cord injury disrupts ascending and descending neural signals causing sensory and motor dysfunction below the injury. Neuromodulation with electrical stimulation is used in both clinical and research settings to induce neural plasticity and improve functional recovery following injury. However, the mechanisms by which electrical stimulation affects recovery remain unclear. In this study we examined the effects of cortical electrical stimulation following injury on transcription at several levels of the central nervous system. We performed a unilateral cervical spinal contusion injury in rats and delivered stimulation for one week to the contralesional motor cortex to activate a descending motor tract.RNA was purified from bilateral subcortical white matter, and 3 levels of the spinal cord. Here we provide the complete data set in the hope that it will be useful for researchers studying electrical stimulation as a therapy to improve recovery from the deficits associated with spinal cord injury.
2021-02-16 | GSE155610 | GEO
Project description:Smart-seq2 of spinal cord motoneurons in spinal cord injury model after dual electrical stimulation with specific frequencies
| PRJNA1016263 | ENA
Project description:Purpose: The goal of this study was to determine the gene expression changes that occur over 7 days in parralyzed muscle in response to isometric contraction elicited by electrical stimulation initiated 4 months after spinal cord injury and to compare such changes to those observed in a normal muscle subjected to overload. Methods: Electrical stimulation of the soleus and plantaris muscle was stimulated in female rats with complete transection of the spinal cord at the interspace between the 9th and 10th thoracic vertebrae. Stimulation was begun 16 weeks after spinal cord transection and produced near-isometric contraction of soleus, plantaris and tibialis anterior. Muscle was analyzed at 1, 2 and 7 days after starting exercise with electrical stimulation. To provide a baseline reference for gene expression at 16 weeks after spinal cord injury, muscle was also analysed from an additional group of spinal cord transected animals. One additional group of animals with a sham-spinal cord injury was included to provide information about gene expression in neurologically intact animals of similar age. In parallel studies, rats underwent bilateral gastrocnemius ablation to overload soleus and plantaris, or a sham ablation as a control. Muscle was analyzed at 1, 3 and 7 days after gastrocnemius ablation or sham-ablation. Gene expression was determined using Affymetrix Rat Exon microarrays. For each group of animals, microarray analysis was performed for soleus muscle for each of 3 separate animals, using one array per animal. Control sammples for the spinal cord injured groups included a group of animals with a Sham-spinal cord injury, and a group of spinal cord injured animals that did not get electrical stimulation. The comparator for determining fold-change expression values was the spinal cord injured group that did not receive electrical stimulation. For each day after gastrocnemius ablation, a control was included that received all procedures needed for this ablation except cutting the distal insertion of the gastrocnemius into the Achilles tendon to control for effects of the surgery on gene expression.
2013-03-30 | E-GEOD-37476 | biostudies-arrayexpress
Project description:The goal of this study is to elucidate the influence of hemisection injury at thoracic spinal cord (T9) and epidural electrical spinal stimulation (L2-S1) on transcriptome of injured thoracic spinal cord. mRNA profiles of spinal cord at 5 days-post injury with or without epidural electrical spinal stimulation (L2-S1) and before injury were generated. Our study represents the detailed analysis of transcriptomes of injured spinal cord with biologic replicates, generated by RNA-seq technology.
2020-05-11 | GSE138637 | GEO
Project description:The characteristics of electrical signals-mediated neural circuits reconstruction remain poorly understood. We initially developed a spinal-muscle synergistic bidirectional electrical stimulation (SBES) protocol to mimic feedforward and feedback electrical signals in spinal sensorimotor circuits. The results indicate that sensorimotor circuits could be precisely reassembled in structure and function levels by 10-20 Hz SBES. To gain mechanistic insights into the reassembly of the spinal sensorimotor circuits with 10-20 Hz SBES, we performed gene expression profiling analysis in motoneurons. Gene ontology (GO) analysis showed that one group of GO terms accounted for a large fraction of the upregulated transcripts. This group includes axon growth-related cellular functions, such as cell adhesion, regulation of cell growth, and cell projection assembly. Statistical analysis of the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways revealed sixteen signaling pathways were involved, two of which were related to the regulation of axonal regeneration (PI3K-Akt signaling pathway and cAMP signaling pathway). This study provides insights into neural signal decoding during spinal sensorimotor circuit reconstruction.
2024-01-15 | GSE222978 | GEO
Project description:High-frequency spinal cord stimulation (HF-SCS) has been proven to be an effective method for treating neuropathic pain, but its specific mechanism of action in spinal cord injury (SCI) remains unclear. This study aims to explore the therapeutic effect of early HF-SCS in a rat model of SCI and its potential molecular mechanism. The SD rat model of T10 spinal cord contusion was established, and stimulation electrodes were implanted epidurally, followed by HF-SCS treatment (movement threshold 40%, frequency 10,000 Hz). The results showed that HF-SCS significantly attenuated SCI-induced neuropathic pain, facilitated functional recovery, and accelerated axonal regeneration and myelin repair. Further mechanism studies indicated that HF-SCS exerts its neuroprotective effect by down-regulating the ROS/p38 MAPK/NF-κB signaling pathway to reduce microglial activation and decrease the release of pro-inflammatory factors; simultaneously, it inhibits the activation of the CXCL10/CXCR3 axis to alleviate central sensitization. This study suggests that early HF-SCS intervention can improve the functional prognosis after SCI by suppressing neuroinflammation and reducing central sensitization, thereby providing a theoretical basis for the treatment of SCI with HF-SCS.
2026-07-14 | GSE332999 | GEO
Project description:Spinal cord stimulation is a promising strategy for functional recovery after spinal cord injury (SCI), but conventional electronic implants pose surgical and long-term risks. Here, we report a biodegradable piezoelectric cryogel (Piezo Gel) that enables programmable electro-neuromodulation without implanted electronics. Mimicking spinal biomechanics, Piezo Gel converts physiological movement into localized endogenous electric fields, while externally applied ultrasound (US) amplifies its electrical output, enabling on-demand in situ programming. In a rat model of acute severe SCI, US-activated Piezo Gel significantly enhanced locomotor recovery, improved Basso–Beattie–Bresnahan (BBB) scores, and promoted bladder functional remodeling. In a mild contusion model, we further implemented a phase-adaptive neuromodulation strategy, shifting from US-driven stimulation during acute immobility to movement-driven stimulation during subacute rehabilitation, aligning with the evolving spinal microenvironment. This sequential programming resulted in substantial restoration of coordinated gait. Together, this work establishes an electronic-free, programmable electro-neuromodulation paradigm that integrates US and physiological motion, offering a clinically translatable approach for SCI repair.
2026-06-21 | GSE326580 | GEO
Project description:Smart-seq2 of spinal cord motor neurons reveals transcriptomic changes in mice with spinal cord injury after synergistic bidirectional electrical stimulation of specific frequencies
| PRJNA924327 | ENA