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The axonal membrane lipid bilayer, also known as the axolemma, is a specialized plasma membrane that encapsulates the axon and is critical for the conduction of action potentials and the maintenance of axonal homeostasis (Bittner et al., 2012). Following a traumatic peripheral nerve injury, the disruption of this lipid bilayer leads to the loss of electrical continuity and initiates Wallerian degeneration of the distal nerve segment (Ghergherehchi et al., 2019). This structure is targeted by chemical fusogens, such as polyethylene glycol (PEG), which act to physically reconnect the severed ends of the axonal membranes. PEG functions by removing the hydration shell from the phospholipid head groups, allowing the lipid bilayers of the proximal and distal stumps to fuse upon contact (Riley et al., 2015). This therapeutic intervention, often referred to as PEG-fusion, aims to restore immediate axonal continuity and prevent the degradation of the distal nerve segment, thereby improving functional recovery outcomes in patients with severe nerve lacerations (Bittner et al., 2016).
Membrane fusion and sealing via chemical fusogens that dehydrate lipid head groups, allowing the lipid bilayers of severed axonal ends to merge and restore cytoplasmic continuity.
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