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.