“ELECTRICAL PROPERTIES AND FUNCTIONAL EXPRESSION OF IONIC CHANNELS IN COCHLEAR INNER HAIR CELLS OF MICE LACKING THE ALPHA10 NICOTINIC CHOLINERGIC RECEPTOR SUBUNIT.

GÓMEZ-CASATI ME; WEDEMEYER C; TARANDA J; LIPOVSEK M; DALAMON V; ELGOYHEN AB; KATZ E.

JARO-JOURNAL OF THE ASSOCIATION FOR RESEARCH IN OTOLARYNGOLOGY

SPRINGER

Lugar: New York; Año: 2009 vol. 10 p. 221 - 232

1525-3961

Cochlear inner hair cells (IHCs) release neurotransmitter onto afferent auditory nerve fibers in response to  sound  stimulation.  During  early  development, synaptic  transmission  is  triggered  by  spontaneous Ca2+   spikes  which  are  modulated  by  an  efferent cholinergic  innervation  to  IHCs.  This  synapse  is inhibitory  and  mediated  by  the  α9α10  nicotinic cholinergic receptor  (nAChR).  After  the  onset  of hearing,  large-conductance  Ca2+-activated  K+   channels are acquired and both the spiking activity and the efferent  innervation  disappear  from  IHCs.  In  this work, we studied the developmental changes in the membrane  properties  of  cochlear  IHCs  from  α10 nAChR  gene  (Chrna10)  “knockout”  mice.  Electrophysiological  properties  of  IHCs  were  studied  by whole-cell recordings in acutely excised apical turnsof the organ of Corti from developing mice. Neither the spiking activity nor the developmental functional expression of voltage-gated and/or calcium-sensitive K+   channels  is  altered  in  the  absence  of  the  α10 nAChR subunit. The present results show that the α10 nAChR  subunit  is  not  essential  for  the  correct establishment of the intrinsic electrical properties of IHCs during development.