The synaptic physiology of cochlear hair cells

Mechanosensory hair cells of the vertebrate inner ear are so-called 'short' receptors that communicate to the central nervous system by way of chemical synapses with afferent neurons. In turn, hair cells are the targets of olivocochlear fibers that carry efferent inhibitory feedback from the brain. These synaptic activities contribute to, or modulate the hair cell's receptor potentials through the gating of associated ion channels. Thus for example, voltage-gated calcium channels open to trigger vesicle fusion and release of transmitter by entry of extracellular calcium. The inward calcium current also depolarizes the membrane and could lead to generation of 'all-or-none' action potentials. However, regenerative depolarization is prevented in most hair cells by prominent voltage-gated potassium conductances that rapidly repolarize the membrane. The magnitude and speed of these delayed potassium conductances determine the size and shape of the resulting receptor potential, and subsequent transmitter release, produced by sound. Efferent feedback is provided by the release of acetylcholine (ACh) from olivocochlear nerve fibers onto outer hair cells in the mammalian cochlea. The hair cell's ACh receptors are ligand-gated cation channels related to the nicotinic receptors of nerve and muscle. Calcium influx through the ACh receptors activates nearby calcium-gated potassium channels, resulting in hyperpolarization and inhibition of the hair cell. Calcium influx during efferent inhibition is regulated by a 'synaptic cistern' that also may act as a calcium store that is triggered by ACh under some conditions.