Inducing Neural Plasticity after Spinal Cord Injury to Recover Impaired Voluntary Movement
Inducing Neural Plasticity after Spinal Cord Injury to Recover Impaired Voluntary Movement
批准号:
9789839
负责人:
Jordan Alexander Borrell
金额:
$3.31万
依托单位国家:
美国
项目类别:
财政年份:
2018
资助国家:
美国
项目状态:
已结题
起止时间:
2018-07-01 至 2020-06-30
关键词:
Action PotentialsActivities of Daily LivingAcuteAddressAdultAffectAftercareAnimal ModelAreaAxonBehaviorBehavior assessmentBehavioralBrainBypassCaringCerebral cortexChemosensitizationChronicClinical ResearchCommunicationContusionsCouplingDevelopmentDevicesDimensionsDistantElectric StimulationFiberFutureGoalsHindlimbHumanImpairmentImplantIndividualInjuryLaboratoriesLesionLower ExtremityLumbar spinal cord structureMapsMedicalMicroelectrodesModelingMotorMotor CortexMotor NeuronsMotor PathwaysMovementMusMuscleNatural regenerationNeurologicNeuronal PlasticityNeuronsNeurostimulation procedures of spinal cord tissueOccupational TherapyParalysedPatientsPerformancePhysical therapyPopulationPre-Clinical ModelPublic HealthRattusRecovery of FunctionRegenerative MedicineResearchRestRodentRoleSensorySignal TransductionSpinalSpinal CordSpinal Cord ContusionsSpinal Cord LesionsSpinal cord injuryStem cellsStimulusSurvivorsSynapsesSynaptic plasticitySystemTechniquesTestingTimeTraumaTraumatic Brain InjuryUnited StatesVentral Horn of the Spinal CordVertebral columnawakeaxon injurybasedesigndisabilityexperienceextracellularfunctional restorationimprovedinsightintraspinal microstimulationmicrostimulationmotor impairmentmotor recoverynerve injuryneurophysiologyneuroprosthesisnovelnovel strategiesnovel therapeuticspre-clinicalpreclinical studyrelating to nervous systemresponserestorationrestorative treatmentyoung adult
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英文摘要
PROJECT SUMMARY/ABSTRACT
Spinal cord injury (SCI) is often an incapacitating neural injury most commonly caused by a traumatic blow to
the spine, damaging the axons that carry sensory and motor signals between the brain and spinal cord, and in
turn, the rest of the body. However, after a contusion to the spinal cord, at least some neuronal fibers above and
below the lesion remain intact. Recently, our laboratory and others have introduced new neuroprosthetic
approaches in an attempt to restore function by utilizing brain-machine-spinal cord interfaces (BMSIs). These
device-based systems use activity-dependent stimulation (ADS) which discriminates neural activity in the intact
motor cortex to use as signals to stimulate motor neurons below the spinal cord lesion. Our long-term goal for
this research is restoration of impaired motor function in the lower limbs following spinal cord injury. The feasibility
of using ADS as a strategy to enhance recovery of function after SCI is supported by the positive results seen in
this laboratory demonstrating the effect of ADS in restoring skilled motor function after traumatic brain injury.
Thus, the overarching hypothesis of this line of research is that ADS will result in enhanced motor recovery in
ambulatory ability after SCI. The proposed project will determine the optimal neurophysiological conditions by
which ADS can facilitate enhanced communication between the cerebral cortex and spinal cord motor neurons.
The project will address three specific aims: 1) Determine the effects of a contusive spinal cord injury on spinal
motor neuron activity, corticospinal coupling, and conduction time in rats 2) determine the optimal spike-stimulus
delay for increasing synaptic efficacy in descending motor pathways using an ADS paradigm in an acute,
anesthetized rat model of SCI, and 3) determine whether spike-triggered ISMS results in improved motor
performance in an ambulatory rat model of SCI. We will test these aims using acute and chronic neurologic
recording and stimulating techniques in both anesthetized and awake, behaving healthy and SCI rodents. The
project is significant because, if realized, this approach may augment concomitant physical and occupational
therapy and result in improved functional abilities. Ultimately, patients may could regain voluntary movement due
to increased synaptic efficacy in corticospinal fibers.
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