The impact of peripheral nerve injury on motor neuron axon collateral contacts onto renshaw cells
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Fix, Caitlin
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Abstract
Motor neuron (MN) firing behavior and recruitment are critical for maintaining proper limb function and movement, a process orchestrated by complex spinal circuits. Dysfunction in these circuits lead to functional deficits like limb discoordination and muscle paralysis. Understanding how peripheral nerve injury (PNI) alters structural circuit connectivity is essential for devising future strategies to maintain circuit function. Our study focuses on the Renshaw cell (RC) circuit, where motoneuron axon collaterals modulate MN firing patterns via inhibitory RC interneurons. We aim to 1) map the normal distribution of motoneuron axon collaterals across RC populations and 2) analyze how peripheral nerve injury reorganizes cholinergic collateral projections onto RCs. To do this, AAV1-mCherry constructs were injected into the medial gastrocnemius (MG) muscle of neonatal rats for retrograde labeling of the MG motor pool. Three months post injection, we transected and repaired the medial gastrocnemius nerve (MGN) or tibial nerve (TN) and allowed one year of recovery. Lumbar spinal cord tissue was collected, sectioned, and labeled using immunohistochemistry (IHC). Cholinergic axon collaterals were labeled using vesicular acetylcholine transporter (VAChT) antibodies and RCs using calbindin antibodies. Sections containing RCs were imaged using confocal microscopy and RCs were subsequently reconstructed in 3D and synaptic densities analyzed. To our surprise, we found that PNI did not alter the distribution of axon collaterals onto RCs, regardless of injury severity. Synaptic density remained unchanged independent of RC morphology and spatial distribution. Limitations in AAV1-mCherry prevented MG motor pool-specific analysis but highlighted labeling methodology for future studies. Additional experiments should be conducted to provide a comprehensive analysis of axon collateral distribution across the entire distal RC dendritic arbor, along with providing supplementary time points to identify transient collateral degeneration or perhaps supernumerary axon growth.
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Undergraduate Research Option Thesis