Reproductive plasticity is the ability of an animal to modulate its reproductive functions in response to environmental changes. For example, Caenorhabditis elegans, a free-living nematode, can adjust the onsets of oogenesis and embryogenesis under harsh environmental conditions, including starvation. However, the molecular mechanisms used to perceive and translate environmental signals into reproductive functional adjustments remain largely uncharacterized. We discovered that in C. elegans, the glutamate receptor homolog MGL-1 initiated reproductive plasticity in response to starvation. A genetic analysis of the mutant gene, mgl-1(tm1811), suggested that starvation delayed the onsets of oogenesis and embryogenesis via MGL-1. Cell-specific rescues of mgl-1 deletion mutants, which used transgenic lines designed to express MGL-1 in different neurons (e.g., RMD, AIA, AIY, and NSM), suggested that only AIY-rescued animals exhibited normal delays in oogenesis and embryogenesis equivalent to those of wild-type animals, suggesting recovery. Furthermore, in AIY neurons, MGL-1 appears to use neuropeptide signaling, rather than glutamate, to translate starvation stimuli into delayed oogenesis and embryogenesis. Our findings, which reveal molecular linkages between starvation signals and reproductive alterations, may provide a basis for understanding energy reallocation mechanisms, as the mgl-1 deletion mutant exhibited more severe reductions in lifespan and fat accumulation than did wild-type animals under starvation conditions. Taken together, MGL-1 is the molecular driver underlying the translation of starvation signals to reproduction plasticity in an AIY neuron-specific manner.