Molecular mechanisms of mechanotransduction in mammalian sensory neurons

Abstract

The somatosensory system mediates fundamental physiological functions, including the senses of touch, pain and proprioception. This variety of functions is matched by a diverse array of mechanosensory neurons that respond to force in a specific fashion. Mechanotransduction begins at the sensory nerve endings, which rapidly transform mechanical forces into electrical signals. Progress has been made in establishing the functional properties of mechanoreceptors, but it has been remarkably difficult to characterize mechanotranducer channels at the molecular level. However, in the past few years, new functional assays have provided insights into the basic properties and molecular identity of mechanotransducer channels in mammalian sensory neurons. The recent identification of novel families of proteins as mechanosensing molecules will undoubtedly accelerate our understanding of mechanotransduction mechanisms in mammalian somatosensation.

Stochastic nanoroughness modulates neuron–astrocyte interactions and function via mechanosensing cation channels

“…5D) and this coincides rather well with the roughness regime on which neurons exhibit decoupling from astrocytes. A role of mechanotransduction in maintaining neuron-astrocyte interactions is further supported by our findings that inhibition of signaling through SACs (Piezo-1, TRPC1, and TRPC 6) using GsMTx4, a peptide extracted from spider venom (34,35), promotes decoupling of neurons from astrocytes even on smooth glass substrates (Fig. 3 H and I) where they normally show strong association (Fig.…”

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Piezo1‐dependent stretch‐activated channels are inhibited by Polycystin‐2 in renal tubular epithelial cells

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