Spinal cord injury alters spinal Shox2 interneurons by enhancing excitatory synaptic input and serotonergic modulation while maintaining intrinsic properties in mouse.
Neural circuitry generating locomotor rhythm and pattern is located in the spinal cord. Most spinal cord injuries (SCI) occur above the level of spinal locomotor neurons; therefore, these circuits are a target for improving motor function after SCI. Despite being relatively intact below the injury, locomotor circuitry undergoes substantial plasticity with the loss of descending control. Information regarding cell-type specific plasticity within locomotor circuits is limited. Shox2 interneurons (INs) have been linked to locomotor rhythm generation and patterning, making them a potential therapeutic target for the restoration of locomotion after SCI. The goal of the present study was to identify SCI-induced plasticity at the level of Shox2 INs in a complete thoracic transection model in adult male and female mice. Whole cell patch clamp recordings of Shox2 INs revealed minimal changes in intrinsic excitability properties after SCI. However, afferent stimulation resulted in mixed excitatory and inhibitory input to Shox2 INs in uninjured mice which became predominantly excitatory after SCI. Shox2 INs were differentially modulated by serotonin (5-HT) in a concentration-dependent manner in uninjured conditions but following SCI, 5-HT predominantly depolarized Shox2 INs. 5-HT
Published In/Presented At
Garcia-Ramirez, D. L., Ha, N. T. B., Bibu, S., Stachowski, N. J., & Dougherty, K. J. (2021). Spinal cord injury alters spinal Shox2 interneurons by enhancing excitatory synaptic input and serotonergic modulation while maintaining intrinsic properties in mouse. The Journal of neuroscience : the official journal of the Society for Neuroscience, 41(27), 5833–5848. Advance online publication. https://doi.org/10.1523/JNEUROSCI.1576-20.2021
Medicine and Health Sciences
Department of Medicine