Changes in the kinetic properties of the a9a10 hair cell nicotinic receptor prolongs olivocochlear inhibition.

CAROLINA WEDEMEYER; ELEONORA KATZ; LUCAS VATTINO; ANA BELEN ELGOYHEN; JIMENA BALLESTERO

Buenos Aires

Workshop; Auditory workshop; 2016

Laboratorio de Fisiología y Genética de Audición (INGEBI-CONICET) e Instituto de Farmacología, Facultad de Medicina, Universidad de Buenos Aires.

Medial olivocochlear (MOC) fibers innervate the cochlear outer (OHCs) hair cells and alsotransiently during development, the inner hair cells (IHCs). The MOC-hair cell synapse ischolinergic, inhibitory and is mediated by a9a10 nicotinic receptors (nAChR). In mice bearing apoint mutation in the a9 nAChR subunit (Kin), in-vivo cochlear efferent-mediated inhibition isdramatically lengthened and enhanced(Taranda 2009). We now investigated whether there arechanges in the short-term plasticity properties (STP) ofMOC-hair cells synapses that could accountfor this enhanced efferent suppression. Evoked synaptic currents were recorded in IHCs and OHCsof isolated mouse organs of Corti.MOC-OHC synapses from Kin mice significantly facilitated upon20 and 40 Hz stimulation (p2/p1- 20Hz= 2.6; p2/p1- 40Hz= 3.2; n=4-8). The probability of releaseincreased during the trains, whereas the size of the events remained stable suggesting a presynapticorigin. Moreover, stimulation of MOC fibers at 80 Hz for 10 s resulted inpostsynaptic responses oflonger duration and slower onset times in both OHCs and IHCs from Kin mice (n=8-16). Inaccordance,preliminary experimentsshow that efferent inhibition of calcium action potentials is morepotent in IHCs from kin mice.We conclude that the alteration in the STP patterns of MOC-hair cellsynapses caused by the mutation could contribute to the observed changes in the dynamics of in-vivocochlear efferent inhibition.