5.1 From receptor potential to spike

The mechanism that turns the IHC’s depolarization into auditory-nerve spikes runs through the ribbon synapse — a structure unique to a few sensory cells, including IHCs, vestibular hair cells, and retinal photoreceptors. Each IHC has 10–30 ribbon synapses on its basal pole, each one contacting a different auditory-nerve fiber. A ribbon synapse is a specialized structure: a single presynaptic density (the ribbon) that tethers a large array of synaptic vesicles in close proximity to the active zone where Ca²⁺-triggered release occurs.

When the IHC depolarizes, voltage-gated Ca²⁺ channels open near the ribbon, Ca²⁺ flows in, and vesicles release glutamate into the synaptic cleft. The released glutamate binds AMPA receptors on the postsynaptic auditory-nerve terminal. If enough AMPA receptors open quickly enough, the spiral-ganglion neuron’s terminal depolarizes past threshold and the fiber fires a spike.

This sounds like a standard chemical synapse, but it is not. Ribbon synapses can release vesicles continuously at rates approaching 1000 per second per ribbon, with sub-millisecond timing precision. Conventional synapses cannot. The ribbon serves as a vesicle conveyor, keeping the active zone primed even under sustained depolarization. This is what gives the auditory system its exceptional temporal fidelity.