Electrical Properties and Functional Expression of Ionic Channels in Cochlear Inner Hair Cells of Mice Lacking the alpha10 Nicotinic Cholinergic Receptor Subunit."

GOMEZ CASATI ME; WEDEMEYER C; TARANDA J; LIPOVSEK M; DALAMÓN V; ELGOYHEN AB; KATZ E

JARO-JOURNAL OF THE ASSOCIATION FOR RESEARCH IN OTOLARYNGOLOGY

SPRINGER

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 á9á10 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 á10 nAChR gene (Chrna10) “knockout” mice. Electrophysiological properties of IHCs were studied by whole-cell recordings in acutely excised apical turns of 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 á10 nAChR subunit. The present results show that the á10 nAChR subunit is not essential for the correct establishment of the intrinsic electrical properties of IHCs during development.2+ spikes which are modulated by an efferent cholinergic innervation to IHCs. This synapse is inhibitory and mediated by the á9á10 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 á10 nAChR gene (Chrna10) “knockout” mice. Electrophysiological properties of IHCs were studied by whole-cell recordings in acutely excised apical turns of 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 á10 nAChR subunit. The present results show that the á10 nAChR subunit is not essential for the correct establishment of the intrinsic electrical properties of IHCs during development.