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Increased synaptic turnover in injured cortical axons: exploring the role of SARM1 ablation
Ensieh Izadi1, William Bennett1, Jessica Collins1
1Wicking Dementia Research and Education Centre, University of Tasmania, Hobart, TAS, Australia.
Introduction:
Programmed axon degeneration significantly affects neural connectivity, however, the underlying mechanisms remain poorly understood, particularly in cortical regions. Sterile Alpha and TIR motif-containing protein 1 (SARM1) is a known regulator of axon degeneration in the peripheral nervous system, but its role in cortical axon plasticity, particularly during injury conditions, remains unclear. This study examined the role of SARM1 in synaptic connectivity and remodelling in the adult sensory-motor cortex under normal physiological conditions and following acute axonal injury.
Methods:
Adult male Thy1-GFP-M mice (3-12 months) expressing EGFP in excitatory neurons were also either wild-type (WT-GFP) or null for SARM1 (SARM1KO-GFP). Using in vivo multiphoton microscopy, long cortical axon segments (~335 μm ± 140 μm), with terminaux and en passant synaptic boutons in the upper layers of the cortical neuropil, were repeatedly imaged at 48-h intervals to assess axon morphology, synaptic density, and synaptic turnover in the presence and absence of SARM1.
Results:
Without injury, axon morphology, synaptic density, and turnover were similar between WT and SARM1KO groups, suggesting that SARM1 is not necessary for maintaining baseline cortical synaptic connectivity. Following axotomy by laser lesion, the non-degenerating proximal axon (still connected to the soma) showed significant changes in synaptic plasticity, with an increased rate of loss of synapses.
Discussion:
Our findings suggest that SARM1 plays no role in the remodelling of synapses in the proximal axon after an acute axonal injury.
