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Direct Ryanodine Receptor-2 Knockout in Primary Afferent Fibers Modestly Affects Neurological Recovery after
Ben C Orem1,2, Johnny R Morehouse1, Spencer Ames1
1Kentucky Spinal Cord Injury Research Center, University of Louisville, School of Medicine, Louisville, Kentucky, USA.
Neurotrauma Reports
|November 7, 2022
Summary
Neuronal ryanodine receptors (RyR) are crucial for brain function. Knocking out RyR2 in sensory neurons after spinal cord injury (SCI) did not affect axon degeneration but worsened locomotor recovery, suggesting a modest role for RyR2 in SCI recovery.
Area of Science:
- Neuroscience
- Cellular Biology
- Genetics
Background:
- Neuronal ryanodine receptors (RyR) regulate calcium release, impacting synaptic plasticity, learning, and memory.
- RyR dysfunction is implicated in neurodegeneration and impaired neurological recovery after spinal cord injury (SCI).
Purpose of the Study:
- To investigate the specific role of RyR2 in axonal fate and functional recovery following SCI.
- To determine if RyR2 in dorsal root ganglion neurons directly influences outcomes after SCI.
Main Methods:
- Generated RyR2 knockout (KO) mice by breeding Advillin-Cre: tdTomato (Ai9) reporter mice with floxed RyR2 mice.
- Induced contusive SCI in adult RyR2 KO and control mice, analyzing axonal degeneration and functional recovery using in vivo imaging and behavioral tests.
Main Results:
- RyR2 KO in primary afferents did not significantly alter axonal degeneration post-SCI.
- RyR2 KO mice exhibited worsened locomotor scores but showed only subtle gait differences compared to controls.
- Further analyses of axonal regeneration and lumbar afferent function revealed no significant group differences.
Conclusions:
- Direct RyR2 deletion in dorsal column primary afferents does not impact axonal degeneration after SCI.
- RyR2 in primary afferents plays a modest role in neurological recovery after spinal cord injury, primarily affecting motor function.
