All aspects of sound information are encoded and transmitted to the brain through synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) in the inner ear. Each IHC is connected to 10-20 SGNs through single synaptic contacts. IHCs release glutamate upon stimulation, activating AMPA receptors that are present in postsynaptic densities (PSDs) of SGNs. EPSCs at these synapses are ~20 times larger than mEPSCs in the brain, whereas PSDs are 5-10 times larger than brain PSDs. We hypothesize that these large PSDs enable large synaptic responses with low receptors saturation. To test this, we implemented a “glutamate uncaging” method, where glutamate can be released on individual PSDs with high temporal and spatial control. EPSCs activated on SGNs were recorded with the patch clamp technique. Stimulating with high laser power, saturating AMPA responses were obtained, with 5 times larger amplitude than mean EPSCs. This implies that during synaptic transmissionAMPA receptors operate in low saturation. Analyzing rise times of uncaging responses, we observed faster kinetics with larger responses. In contrast, EPSCs presented fast rise times with amplitudes that varied 10-fold. This suggests that EPSCs are produced by a short glutamate transient. Low saturation and fast glutamate clearance allows for high frequency signaling at this synapse.
