Short-term synaptic plasticity at the medial olivocochlear hair cell synapse in ¦Á9L9¨ªT knock-in mice"

BALLESTERO J; ALVAREZ HEDU¡§¢N F; FUCHS PA; KATZ E; ELGOYHEN AB

Congreso; 34th Midwinter Meeting, Association for Research in Otolaryngology; 2012

Cochlear amplification is regulated by medial olivocochlear (MOC) neurons that synapse onto outer hair cells (OHCs). This synapse is mediated by the ¦Á9¦Á10 nicotinic receptor (nAChR). We have generated a mouse with a point mutation (L9¡¯T) in the ¦Á9¦Á10 nAChR that produces longer-lasting inhibitory postsynaptic currents (IPSCs) and changes the magnitude and the dynamics of the efferent-mediated inhibition of cochlear responses (Taranda et al. Plos Biology, 2009). Our goal is now to determine if there is a consequent change in the short-term plasticity (STP) properties of the MOC-hair cell synapse. Synaptic activity was recorded in voltage-clamped inner hair cells (IHCs) from excised apical turns of wild-type (wt) or ¦Á9L9¡¯T knock-in (kin) mouse cochleas (P9-11), during electrical stimulation of the MOC fibers. Evoked IPSCs in kin mice had longer decay times and smaller amplitudes. In wt IHCs, prolonged high frequency stimulation produced an increase in the postsynaptic response during the 1st second, followed by depression that produced ~80% decay in the response. In kin mice, peak responses were reached after ~3 sec of stimulation and then decayed by 50%. These results show that changes in the dynamics of the nAChR induce dramatic changes in the MOC-hair cell synapse STP properties.