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Pursley, R.

Publications and source records attributed to Pursley, R..

2 recordsLinked to original sources

A spinal substrate for modular control of natural behavior

Natural behavior unfolds as coordinated sequences of body movements. This organization suggests that behavior may be built from discrete motor patterns, yet how such arrangements are implemented by neural circuits remains unknown. Here, we combined kinematic analysis, muscle recordings, genetically identified cell types, and closed-loop optogenetic perturbations to examine the organizational logic of natural gap-crossing jumps in mice. Jumping was characterized by a series of precisely defined phases and their associated modular motor patterns. The core phases, propulsion and flight, exhibited distinct signatures of neural control, including unique bursts of coordinated hindlimb muscle activity, differential tuning strategies for jump distance, and active requirements for spinal neural drive. Mapping activity across lumbar interneuron populations and functionally screening candidate cell types for their ability to drive coordinated movement revealed that a population of dorsal excitatory dILB6 neurons can autonomously evoke coordinated multi-joint hindlimb flexion characteristic of the jumping flight phase, across behavioral contexts. These findings provide a specific cellular substrate for the long-standing concept of spinal modular motor control: a flexible, preconfigured motor template that the mammalian CNS can recruit and modulate to meet the demands of natural behavior. Highlights- Jumping behavior is organized into discrete phases with stereotyped motor patterns - Each phase contains a distinct signature of body-wide, joint, and muscle coordination - dILB6 spinal interneurons autonomously evoke a triple-flexion hindlimb motor module - dILB6 neurons can shape active jumping behavior

neuroscience↗

A Single Cell Atlas of Spared Tissue Below a Spinal Cord Injury Reveals Cellular Mechanisms of Repair

After spinal cord injury (SCI), the "spared" tissue below the lesion contains undamaged cells that could support or augment recovery, but targeting these cells requires a clearer understanding of their injury responses and capacity for repair. Here, we used single nucleus sequencing to profile how each cell type in the lumbar spinal cord changes over time after a thoracic injury. We present an atlas of these dynamic responses and explore two unexpected findings. Amongst neurons, rare cell types expressed a molecular signature of regeneration and amongst microglia, we identified a population of "trauma associated microglia" (TAM). These TAM cells were present in the white matter near degenerating axons and expressed the trophic factors Igf1 and Spp1(OPN). Viral over-expression of Igf1 and Spp1(OPN) expanded the TAM population and promoted the clearance of myelin debris. These findings expose endogenous mechanisms of repair in spared neural tissue, uncovering potential candidates for targeted therapy.

neuroscience↗