Hypoosmotic- and pressure-induced membrane stretch activate TRPC5 channels

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Hypoosmotic- and pressure-induced membrane stretch activate TRPC5 channels.

Transient receptor potential (TRP) channels mediate a wide array of sensory functions. We investigated the role of TRPC5, a poorly characterized channel widely expressed in the central and peripheral nervous system, as a potential osmosensory protein. Here we show that hypoosmotic stimulation activates TRPC5 channels resulting in a large calcium influx. The response to osmotically induced membr...

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Plasma Membrane Mechanical Stress Activates TRPC5 Channels

Mechanical forces exerted on cells impose stress on the plasma membrane. Cells sense this stress and elicit a mechanoelectric transduction cascade that initiates compensatory mechanisms. Mechanosensitive ion channels in the plasma membrane are responsible for transducing the mechanical signals to electrical signals. However, the mechanisms underlying channel activation in response to mechanical...

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TRPC5 channels participate in pressure-sensing in aortic baroreceptors

Blood pressure is maintained within a normal physiological range by a sophisticated regulatory mechanism. Baroreceptors serve as a frontline sensor to detect the change in blood pressure. Nerve signals are then sent to the cardiovascular control centre in the brain in order to stimulate baroreflex responses. Here, we identify TRPC5 channels as a mechanical sensor in aortic baroreceptors. In Trp...

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Hypoosmotic stimuli activate a chloride conductance in rat taste cells.

The oral cavity is subjected to a wide range of osmotic conditions, yet little is known about how solution osmolarity affects performance of the gustatory system. In order to elucidate the mechanism by which hypoosmotic stimuli affect the peripheral taste system, I have attempted to characterize the effects of hypoosmotic stimuli on individual rat taste receptor cells (TRCs) using whole-cell pa...

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ژورنال

عنوان ژورنال: The Journal of Physiology

سال: 2008

ISSN: 0022-3751

DOI: 10.1113/jphysiol.2008.161257