FIGURE 5.

The ClC Cl^– channel clh-1 is needed in the Amphid Sheath (Amsh) glia of C. elegans for response to nose touch by mediating GABA signaling. (A) Schematic representation of nose touch response in C. elegans ASH neurons. Using the Ca²⁺ sensor GCaMP-6s, in Fernandez-Abascal et al. (2022) we showed that nose touch stimulation induces Ca²⁺ transients (shown as change in GCaMP6s fluorescence over the baseline, ΔF/F,%) in the ASH nose touch sensory neuron mediated by the activation of DEG/ENaC channel deg-1. Stimulation with a second touch induces reduced Ca²⁺ transients, indicating that adaptation to touch occurs in this nematode receptor. Adaptation is prevented by knockout of the glial channel clh-1 or of unc-25, the GABA synthetic enzyme glutamate decarboxylase, as well as treatment with the GABA_A receptor antagonist bicuculline. These data, together with others presented in Fernandez-Abascal et al. (2022) support the idea that clh-1 is needed for glia-to-neuron GABA signaling that mediates neuronal adaptation. ASH neurons’ adaptation is in turn needed for behavioral response to nose touch. (B) Schematic representation of nose touch response in C. elegans Amsh glia. Nose touch induces Ca²⁺ transients also in the Amsh glia, indicating that these cells are mechanosensitive. The Ca²⁺ transients elicited by nose touch in Amsh glia are not dependent on clh-1. (C) Depiction of glia-to-neuron cross talk in the nose touch receptors of C. elegans. Longitudinal section of the Amphid sensory organ of C. elegans showing the Amsh glia (green) wrapping around the terminal dendrites of 12 pairs of amphid sensory neurons; here only the ASH touch neuron’s dendrite is shown for simplicity. In addition, glial Amphid Socket cells (Amso, in blue) wrap around the most distal part of the sensory dendrites. In Amsh glia, clh-1 is needed for glia-to-neuron GABA signaling by providing the Cl^– ions that permeate through the neuronal GABA_A receptor. GABA is postulated to be released via vesicle fusion, though other modes of GABA release may exist in Amsh glia, including bestrophin channels (Wang et al., 2022). A yet to be identified mechanosensitive channel (depicted here in orange) is expressed in Amsh glial cells and is likely responsible for these cells’ mechanosensitivity [adapted from Fernandez-Abascal et al. (2022)].