Abstract:
:Mechanoelectric transducer (MET) channels, located near stereocilia tips, are opened by deflecting the hair bundle of sensory hair cells. Defects in this process result in deafness. Despite this critical function, the molecular identity of MET channels remains a mystery. Inherent channel properties, particularly those associated with permeation, provide the backbone for the molecular identification of ion channels. Here, a novel channel rectification mechanism is identified, resulting in a reduced pore size at positive potentials. The apparent difference in pore dimensions results from Ca(2+) binding within the pore, occluding permeation. Driving force for permeation at hyperpolarized potentials is increased because Ca(2+) can more easily be removed from binding within the pore due to the presence of an electronegative external vestibule that dehydrates and concentrates permeating ions. Alterations in Ca(2+) binding may underlie tonotopic and Ca(2+)-dependent variations in channel conductance. This Ca(2+)-dependent rectification provides targets for identifying the molecular components of the MET channel.
journal_name
J Neurophysioljournal_title
Journal of neurophysiologyauthors
Pan B,Waguespack J,Schnee ME,LeBlanc C,Ricci AJdoi
10.1152/jn.01178.2011subject
Has Abstractpub_date
2012-05-01 00:00:00pages
2408-20issue
9eissn
0022-3077issn
1522-1598pii
jn.01178.2011journal_volume
107pub_type
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