Structural neuroplasticity after sleep loss modifies behavior and requires neurexin and neuroligin

Structural neuroplasticity (changes in the size, strength, number, and targets of synaptic connections) can be modified by sleep and sleep disruption. However, the causal relationships between genetic perturbations, sleep loss, neuroplasticity, and behavior remain unclear. The C. elegans GABAergic DVB neuron undergoes structural plasticity in adult males in response to adolescent stress, which rewires synaptic connections, alters behavior, and is dependent on conserved autism-associated genes NRXN1/nrx-1 and NLGN3/nlg-1. We find that four methods of sleep deprivation transiently induce DVB neurite extension in day 1 adults and increase the time to spicule protraction, which is the functional and behavioral output of the DVB neuron. Loss of nrx-1 and nlg-1 prevent DVB structural plasticity and behavioral changes at day 1 caused by adolescent sleep loss. Therefore, nrx-1 and nlg-1 mediate the morphologic and behavioral consequences of sleep loss, providing insight into the relationship between sleep, neuroplasticity, behavior, and neurologic disease. [Display omitted] •Adolescent sleep deprivation induces GABAergic neurite outgrowth in adult C. elegans•Sleep loss alters the synapses of the GABAergic neuron and changes behavior•Sleep loss induced morphologic/behavioral changes require neurexin and neuroligin•Adolescent sleep deprivation induced neurite outgrowth is transient in adulthood Behavioral neuroscience; Molecular neuroscience; Cellular neuroscience