A point mutation in the α9α10 nAChR alters short-term synaptic plasticity of medial olivocochlear- hair cell (MOC-HC) synapses

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

Mar del Plata

Congreso; XXX Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias (SAN); 2015

Sociedad Argentina de Investigación en Neurociencias (SAN)

IHCs convey acoustic information to the central nervous system while OHCs areresponsible for the mechanical amplification of sound. IHCs receive a transient MOCinnervation since birth to the onset of hearing, while MOC fibers synapse onto OHCs fromthe first postnatal week throughout adulthood. The MOC-HC synapse is inhibitory andmediated by α9α10 nicotinic receptors (nAChRs). We analyzed the properties of synaptictransmission of a knock-in mouse (Kin) with a point mutation in the α9 nAChR subunit(L9´T) that prolongs MOC inhibition (Taranda et. al 2009). Synaptic currents (IPSCs) wererecorded in IHCs and OHCs of isolated mouse cochleas at postnatal day 9-13 duringelectrical stimulation of MOC fibers. In previous studies we showed that high frequencystimulation causes synaptic depression in MOC-IHC synapses, whereas it causes facilitationin MOC-OHC synapses. We found that in both wt and Kin IHCs, 100Hz-trains applied to theMOC fibers caused depression of IPSC amplitudes (S10/S1: 21% and 10% in Kin and wtmice, respectively) whereas 10Hz-trains caused depression only in Kin mice (S10/S1:60%).Accordingly, the ready releasable pool size was smaller in Kin mice (wt:3.7±0.9Kin:2.7±0.8). Preliminary experiments in OHCs show that high frequency stimulation (40-80Hz) caused 3-fold more facilitation in Kin than in wt mice. These results show that amodification in the postsynaptic nAChR alters the short term plasticity pattern of MOC-HCsynapses.Support UBA & ACyPT