Abstract
Stretch-activated afferent neurons, such as those of mammalian muscle spindles, are essential for proprioception and motor co-ordination, but the underlying mechanisms of mechanotransduction are poorly understood. The dorsal bipolar dendritic (dbd) sensory neurons are putative stretch receptors in the Drosophila larval body wall. We have developed an in vivo protocol to obtain receptor potential recordings from intact dbd neurons in response to stretch. Receptor potential changes in dbd neurons in response to stretch showed a complex, dynamic profile with similar characteristics to those previously observed for mammalian muscle spindles. These profiles were reproduced by a general in silico model of stretch-activated neurons. This in silico model predicts an essential role for a mechanosensory cation channel (MSC) in all aspects of receptor potential generation. Using pharmacological and genetic techniques, we identified the mechanosensory channel, DmPiezo, in this functional role in dbd neurons, with TRPA1 playing a subsidiary role. We also show that rat muscle spindles exhibit a ruthenium red-sensitive current, but found no expression evidence to suggest that this corresponds to Piezo activity. In summary, we show that the dbd neuron is a stretch receptor and demonstrate that this neuron is a tractable model for investigating mechanisms of mechanotransduction.
Highlights
Mechanotransduction is key to essential sensory functions, such as touch and proprioception
Combining electrophysiological recordings of the receptor potential with genetics, pharmacology and mathematical modelling, we examine the mechanosensory mechanism, and in particular the role of two candidate mechanotransduction proteins known to be expressed in dbd neurons: TRPA1 and DmPiezo [13, 14]
By mechanically stimulating the cell, we were able to obtain recordings of the dbd neuron receptor potential generated in response to a stretch stimulus
Summary
Mechanotransduction is key to essential sensory functions, such as touch and proprioception. Crayfish muscle stretch receptors and vertebrate muscle spindles show strikingly similar electrophysiological responses to stretch stimuli [7, 8, 9] These responses can be described and reproduced in biophysical models [10, 11], which potentially provide predictive tools for identifying the proteins of the mechanosensory response. The genetic tractability of Drosophila and the accessibility of its dbd neurons potentially provide a route to understanding the molecular mechanisms of stretch receptor mechanotransduction. Combining electrophysiological recordings of the receptor potential with genetics, pharmacology and mathematical modelling, we examine the mechanosensory mechanism, and in particular the role of two candidate mechanotransduction proteins known to be expressed in dbd neurons: TRPA1 and DmPiezo [13, 14]
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