Glia Modulate a Neuronal Circuit for Locomotion Suppression during Sleep in C. elegans

Publication date: 6 March 2018
Source:Cell Reports, Volume 22, Issue 10
Author(s): Menachem Katz, Francis Corson, Shachar Iwanir, David Biron, Shai Shaham
Glia have been suggested to regulate sleep-like states in vertebrates and invertebrates alike. In the nematode Caenorhabditis elegans, sleep is associated with molting between larval stages. To understand if glia modulate neural circuits driving sleep in C. elegans larvae, we ablated the astrocyte-like CEPsh glia. We found that glia-ablated animals exhibit episodes of immobility preceding sleep, prolonged sleep, molting-independent short-duration locomotory pausing, and delayed development. CEPsh glia ensheath synapses between the sleep-associated ALA neuron and its postsynaptic partner AVE, a major locomotion interneuron. While AVE calcium transients normally correlate with head retraction, glia ablation results in prolonged calcium transients that are uncoupled from movement. Strikingly, all these glia ablation defects are suppressed by the ablation of ALA. Our results suggest that glia attenuate sleep-promoting inhibitory connections between ALA and AVE, uncovering specific roles for glia in sleep behavior. We propose that similar mechanisms may underlie glial roles in sleep in other animals.

Graphical abstract

Teaser

Sleep is characterized by reduced mobility. How neural circuits drive sleep-associated locomotion inhibition is not known. Here, Katz et al. demonstrate that neuron-associated glial cells prevent unintended sleep entry by inhibiting neuronal connections that promote sleep-related locomotion attenuation.


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