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The nicotinic acetylcholine receptor subunit alpha-10 (α10) is a structural component of heteromeric α9α10 nAChRs primarily expressed in cochlear hair cells, where it assembles with α9 subunits to form ligand-gated ion channels essential for olivocochlear efferent neurotransmission. These receptors respond to acetylcholine released from olivocochlear terminals, enabling calcium influx that activates small-conductance potassium channels, hyperpolarizes outer hair cells, and suppresses cochlear amplification to protect against noise or enhance signal detection. Unlike homomeric α9 receptors, which produce weak currents and fail to support normal synaptic function or innervation in vivo, α10 is required for robust channel properties, proper efferent synapse development, and maintenance of auditory circuit integrity, as evidenced by knockout mice showing disorganized innervation, failed distortion product suppression, and residual low-amplitude responses. α10 expression extends to select brain regions including frontal cortex, medulla oblongata, and hippocampus, with compensatory regulation alongside α7 and α9 subunits, and presence in neuronal mitochondria. Although not directly linked to specific diseases in the data, disruptions impair auditory processing, highlighting its role in sensory physiology rather than broad therapeutic targeting.
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