Olivocochlear system

The olivocochlear system is part of the auditory system and represents a method of descending control. This control is expressed via both a neural and a mechanical basis. Thus, one portion of the olivocochlear system produces synapses with the dendrites of the Type I spiral ganglion cells projecting to the inner hair cells. The second portion synapses directly with the outer hair cells, and controls the mechanical state of these motile elements. The outer hair cells are considered the cellular elements of the cochlear amplifier. By controlling the mechanical state of these motile elements, basilar membrane displacement and velocity are either suppressed or enhanced. A second theory of olivocochlear function posits its modulation of cochlear output via interactions with hair cells that result in altered stereocilia oscillations and/or motions that then feed into tectorial membrane mechanics, thus altering hair cell transduction.

Anatomy of olivocochlear innervation to hair cells: The olivocochlear system is commonly split into medial and lateral systems based on the location of the cell bodies of origin- medial or lateral to the medial superior olive (MSO). The lateral olivocochlear system (LOCS) has its cell bodies in and/or around the lateral superior olive (depending on the species), while the medial olivocochlear system (MOCS) has its cell bodies in the ventral nucleus of the trapezoid body, a periolivary, loose ensemble of cells in the ventral portions of the superior olive. The lateral system terminates on the dendrites of the Type 1 spiral ganglion cells, whereas the medial system directly contacts the outer hair cells. The brain is therefore able to influence the output of both sets of receptor cells.

Olivocochlear activity at outer hair cells: All currently known activity of the olivocochlear system is via a nicotinic class neurotransmitter receptor complex that is coupled with a calcium-activated potassium channel. Together, these systems generate an unusual synaptic response to stimulation from the brain. The olivocochlear synaptic terminals contain various neurotransmitters and neuroactive peptides. The major neurotransmitter employed by the olivocochlear system is acetylcholine (ACh), although gamma-aminobutyric acid (GABA) is also localized in the terminals. ACh release from the olivocochlear terminals activates an evolutionarily ancient cholinergic receptor complex composed of the nicotinic alpha9 doi:10.1016/0092-8674(94)90555-Xand alpha10 [1] subunits. While these subunits create an ligand-gated ion channel that is especially permeable to calcium and monovalent cations doi:10.1016/S0378-5955(99)00214-2, the cellular response of the outer hair cells to ACh activation is hyperpolarizing, rather then the expected depolarizing response. This comes about due to the rapid activation of an associated potassium channel. This channel, the apamin sensitive, small conductance SK2 potassium channel, is activated by calcium that is likely released into the cytoplasm via calcium-induced calcium release from calcium stores within the subsynaptic cisternae as a response to incoming calcium from the nicotinic complex [2]. However, it has not been ruled out that some incoming calcium through the nicotinic alpha9alpha10 channel may also directly activate the SK channel. Electrophysiological responses recorded from outer hair cells following ACh stimulation therefore show a small inward current (carried largely by incoming calcium via the acetylcholine receptor) that is immediately followed by a large outward current, the potassium current, that hyperpolarizes the outer hair cell.

Consequences of olivocochlear activity: The role of the lateral olivocochlear efferent system is unclear, although one report [3] has demonstrated a loss of balanced sensitivity between the ears following surgical lesion of the LOCS. There are three main hypotheses concerning the role of the medial olivocochlear efferent system: protection from loud sounds which can cause a temporary threshold shift, improving detection of sounds in noise (the "cocktail" effect), and controlling cochlear mechanics and the cochlear amplifier.