Abstract
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.
Highlights
Stress is defined as any challenge to the maintenance of homeostasis that produces adaptive behavioral and/or physiological responses [1]
Levels of Dopamine Differ in Corazonin Deficient Flies Given the observation that flies with altered corazonin neuronal function differ in their hyperactivity and normal locomotor activity profiles, we investigated the possibility that corazonin may be acting in concert with other hormones to shape these behavioral responses
Our observations implicate corazonin neurons as a critical anatomical locus that participates in stress response, we cannot rule out the possibility that the phenotypes associated with corazonin neuronal manipulations reflect changes in an unknown co-transmitter
Summary
Stress is defined as any challenge to the maintenance of homeostasis that produces adaptive behavioral and/or physiological responses [1]. There is significant central processing of these responses to stress, allowing for differential controls targeting different behavioral and physiological outputs. A major action of CRF is the control of ACTH secretion, which in turn increases the production of cortisol, which produces a multiplicity of different responses dependent upon cellular identity [3]. Another prominent action of CRF is the stress-induced inhibition of Gonadotropin releasing hormone (GnRH) signaling [4]
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