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Neuropharmacology. 2015 Jul;94:80-6. doi: 10.1016/j.neuropharm.2014.12.007. Epub 2014 Dec 18.

ASICs and mammalian mechanoreceptor function.

Author information

1
Department of Neuroscience, Max Delbrück Center for Molecular Medicine, Robert-Rössle Straße 10, D-13125 Berlin, Germany.
2
Dept. of Pharmacology, University of Cambridge, Tennis Court Rd., Cambridge CB2 1PD, United Kingdom.
3
Dept. of Pharmacology, University of Cambridge, Tennis Court Rd., Cambridge CB2 1PD, United Kingdom. Electronic address: es336@cam.ac.uk.
4
Department of Neuroscience, Max Delbrück Center for Molecular Medicine, Robert-Rössle Straße 10, D-13125 Berlin, Germany. Electronic address: glewin@mdc-berlin.de.

Abstract

It is well established that some members of the Deg/ENaC super family of amiloride sensitive ion channels can participate directly in the transduction of mechanical stimuli by sensory neurons in invertebrates. A large body of work has also implicated the acid sensing ion channels family (ASIC1-4) as participants in regulating mechanoreceptor sensitivity in vertebrates. In this review we provide an overview of the physiological and genetic evidence for involvement of ASICs in mechanosensory function. On balance, the available evidence favors the idea that these channels have an important regulatory role in mechanosensory function. It is striking how diverse the consequences of Asic gene deletion are on mechanosensory function with both gain and loss of function effects being observed depending on sensory neuron type. We conclude that other, as yet unknown, molecular partners of ASIC proteins may be decisive in determining their precise physiological role in mechanosensory neurons. This article is part of the Special Issue entitled 'Acid-Sensing Ion Channels in the Nervous System'.

KEYWORDS:

ASICs; Ion channels; Mechanoreceptor; Mechanotransduction; Nociceptor; Potassium channels; Touch

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