Summary: Neurons change dramatically over the life-span, including developmentally and as a function of circadian and sleep::wake cycles. Understanding the molecular mechanisms of synaptic change under these conditions may provide insight into the fundamentals of nervous system function. The nematode Caenorhabditis elegans exhibits a developmental, circadian regulated sleep-like state---lethargus, ideal for this study. Plasticity at the neuromuscular junction during lethargus was examined pharmacologically, genetically, and optogenetically. Our findings suggested the following: (1) alterations in transmission at the neuromuscular junction depend on developmental timing and not behavioral state; (2) GABAergic synaptic transmission is reduced during lethargus; (3) a post-synaptic mechanism contributes to the reduced transmission during lethargus. Further, genetic studies aimed towards mechanism found that the alteration in transmission is genetically conferred. That is, both an EMS mutant and a naturally occurring strain without plasticity during lethargus were obtained.