AAV9-mediated KCC2 upregulation enhances functional recovery following cervical spinal cord injury.

ABSTRACT: Following traumatic cervical spinal cord injury (SCI), injury-induced functional changes within the perilesional forelimb circuits are an important cause of neurological dysfunction. K⁺/Cl^- cotransporter 2 (KCC2) is a neuron-specific transmembrane protein essential for inhibitory neurotransmission. Reduced KCC2 expression post-SCI disrupts the excitatory/inhibitory ratio in spinal interneurons and blocks supraspinal neurotransmission. Recent advances in AAV9-based gene therapies present a promising approach to upregulate KCC2 and restore functional communication in the injured spinal circuits. This study aims to characterize the neurophysiological changes in a rodent model of bilateral contusion-compression cervical SCI and to assess the functional impact of KCC2 gene

SUBMITTER: Zavvarian MM 

PROVIDER: S-EPMC12540893 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature