Spinal Cord Injury Research

This study shows that chronic spinal cord injury reduces presynaptic inhibition via PBSt afferents, but step-training restores it through activity-dependent plasticity in decerebrated rats.

This study uses functional ultrasound imaging to show that spinal cord hemodynamic responses to epidural stimulation reflect changes in spinal circuitry organization based on stimulation parameters.

This study combines AAV-ADAMTS4 gene therapy with hindlimb rehabilitation to enhance functional recovery after spinal cord injury by degrading CSPGs.

This study examines how the dorsal horn of primates reorganizes after a hand-specific deafferentation injury, revealing changes in afferent and cortical input connections and terminal bouton sizes.

This study examines how buspirone affects the H-reflex in mice with acute spinal cord injury, finding a biphasic effect with initial depression followed by enhancement of reflex excitability.

This study shows that a mature human immune system in humanized mice, developed over 3-4 months, leads to worse spinal cord injury outcomes due to increased neuroinflammation.

This study compares molecular and histologic outcomes of spinal cord injury in spiny mice (Acomys cahirinus) and C57BL/6 mice, finding reduced inflammation and fibrosis in Acomys.

This study shows that in rats, the somatosensory corticospinal tract (S1 CST) sprouts beyond its normal range after a dorsal root/dorsal column spinal injury, similar to findings in macaques.

This paper introduces a novel method to assess motor behavior in rodents by integrating electrophysiological, biomechanical, and behavioral metrics during therapeutic interventions.

This study shows that exercise reduces spasticity after spinal cord injury by restoring chloride homeostasis via the BDNF-KCC2 pathway.

This study shows that a combinatorial biomaterials strategy with rapamycin and Schwann cells improves functional recovery and reduces fibrosis in rat spinal cord injury.

The paper examines how chronic spinal cord injury alters gene co-expression networks of ion channels and receptors in mouse lumbar spinal cord, revealing cell-type-specific changes in correlation patterns.