Appropriate adjustment of neuronal activity is crucial for development and maintenance of neural circuits, and it is accomplished via various forms of homeostatic plasticity. Recent studies revealed that homeostatic plasticity occurs as structural and functional changes of the axon initial segment (AIS), which is a specialized axonal region involved in initiation of action potentials. This plasticity at the AIS has the most direct impact on neuronal excitability, and should be an efficient mechanism of regulating activity in a circuit. In this symposium, I will summarize our findings on this plasticity, and discuss its contribution to the maintenance of homeostasis of auditory neurons.
In avian cochlear nucleus, deprivation of auditory inputs increased length of the AIS without changes in density of voltage-gated Na+ channels, causing an increase of Na+ conductance and augmenting excitability of neurons. Notably, this elongation accompanied subtype-specific changes in voltage-gated K+ (Kv) channels; Kv1.1 decreased, while Kv7.2 increased, showing a complementary change in their expressions. Kv1.1 has low threshold and rapid kinetics for activation and strongly inhibits firing, while Kv7.2 has slow kinetics and contributes to set the resting potential, indicating that the decrease of Kv1.1 enhances excitability but it is balanced with the increase of Kv7.2 at the rest. Indeed, the resting membrane potential was not altered during the enhancement of excitability. Thus, these structural and functional changes of the AIS cooperatively work, and maintain excitability and resting potential of neurons in cochlear nucleus after deprivation of afferent inputs.