Neuron. 2022 Feb 2;110(3):470-485.e7. doi: 10.1016/j.neuron.2021.11.010. | PubMed

Jesus Fernandez-Abascal¹, Christina K Johnson¹, Bianca Graziano¹, Lei Wang¹, Nicole Encalada¹, Laura Bianchi²

1. Department of Physiology and Biophysics, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
2. Department of Physiology and Biophysics, Miller School of Medicine, University of Miami, Miami, FL 33136, USA. Electronic address: lbianchi@med.miami.edu.

Abstract

In touch receptors, glia and accessory cells play a key role in mechanosensation. However, the mechanisms underlying such regulation are poorly understood. We show, for the first time, that the chloride channel CLH-1 is needed in glia of C. elegans nose touch receptors for touch responses and for regulation of excitability. Using in vivo Ca2+ and Cl- imaging, behavioral assays, and combined genetic and pharmacological manipulations, we show that CLH-1 mediates Cl- flux needed for glial GABA inhibition of ASH sensory neuron function and for regulation of cyclic AMP levels in ASH neurons. Finally, we show that the rat ClC-2 channel rescues the clh-1 nose-touch-insensitive phenotype, underscoring conservation of function across species. Our work identifies a glial Cl- channel as a novel regulator of touch sensitivity. We propose that glial CLH-1 regulates the interplay between Ca2+ and cAMP signaling in ASH neurons to control the sensitivity of the worm's nose touch receptors.

Presented By Jesus Fernandez-Abascal | ORCID iD