AIS structural plasticity allows neurons to adapt their excitability and become resilient to several physiological and pathological conditions. Short hypoxia as well as hibernation state trigger reversible AIS plasticity. The reversible AIS dismantling observed following nerve crush might be protective by facilitating mitochondrial transport into the distal axon, thereby promoting regeneration. However, more prolonged injury causes an irreversible disassembly of the AIS. While AIS plasticity is protective in some cases, it might also become maladaptive. Increased AIS length caused by lowered network activity effectively helps in restoring activity level in the network by making neurons more excitable. However, this increased neuronal excitability might also contribute to overall network E/I imbalance and instability.
