All organisms are confronted with dynamic environmental changes that challenge homeostasis, which is the operational definition of stress. Stress produces adaptive behavioral and physiological responses, which, in the Metazoa, are mediated through the actions of various
hormones. Based on its associated phenotypes and its expression profiles, a candidate stress
hormone in Drosophila is the
corazonin neuropeptide. We evaluated the potential roles of
corazonin in mediating stress-related changes in target behaviors and physiologies through genetic alteration of
corazonin neuronal excitability. Ablation of
corazonin neurons confers resistance to metabolic, osmotic, and oxidative stress, as measured by survival. Silencing and activation of
corazonin neurons lead to differential lifespan under stress, and these effects showed a strong dependence on sex. Additionally, altered
corazonin neuron physiology leads to fundamental differences in locomotor activity, and these effects were also sex-dependent. The dynamics of altered locomotor behavior accompanying stress was likewise altered in flies with altered
corazonin neuronal function. We report that
corazonin transcript expression is altered under
starvation and osmotic stress, and that
triglyceride and
dopamine levels are equally impacted in
corazonin neuronal alterations and these phenotypes similarly show significant sexual dimorphisms. Notably, these sexual dimorphisms map to
corazonin neurons. These results underscore the importance of central peptidergic processing within the context of stress and place
corazonin signaling as a critical feature of neuroendocrine events that shape stress responses and may underlie the inherent sexual dimorphic differences in stress responses.