A Gain-of-Function Mutation in the α9 Nicotinic Acetylcholine Receptor Alters Medial Olivocochlear Efferent Short-Term Synaptic Plasticity.
Wedemeyer, Carolina; Vattino, Lucas G; Moglie, Marcelo J; Ballestero, Jimena; Maison, Stéphane F; Di Guilmi, Mariano N; Taranda, Julian; Liberman, M Charles; Fuchs, Paul A; Katz, Eleonora; Elgoyhen, Ana Belén.
; 38(16): 3939-3954, 2018 Apr 18.
Artigo em Inglês | MEDLINE | ID: mdl-29572431
Short-term synaptic plasticity regulates the level of olivocochlear inhibition to auditory hair cells.
Activation of BK and SK channels by efferent synapses on outer hair cells in high-frequency regions of the rodent cochlea.
Ultrastructure of cisternal synapses on outer hair cells of the mouse cochlea.
The alpha10 nicotinic acetylcholine receptor subunit is required for normal synaptic function and integrity of the olivocochlear system.
Acid-Sensing Ion Channels Activated by Evoked Released Protons Modulate Synaptic Transmission at the Mouse Calyx of Held Synapse.
Adenomatous Polyposis Coli Protein Deletion in Efferent Olivocochlear Neurons Perturbs Afferent Synaptic Maturation and Reduces the Dynamic Range of Hearing.
Onset of cholinergic efferent synaptic function in sensory hair cells of the rat cochlea.
Ca(2+) current facilitation determines short-term facilitation at inhibitory synapses between cerebellar Purkinje cells.