Food deprivation reduces and leptin increases the amplitude of an active sensory and communication signal in a weakly electric fish

5 years ago

Food deprivation reduces and leptin increases the amplitude of an active sensory and communication signal in a weakly electric fish

Energetic demands of social communication signals can constrain signal duration, repetition, and magnitude. The metabolic costs of communication signals are further magnified when they are coupled to active sensory systems that require constant signal generation. Under such circumstances, metabolic stress incurs additional risk because energy shortfalls could degrade sensory system performance as well as the social functions of the communication signal. The weakly electric fish Eigenmannia virescens generates electric organ discharges (EODs) that serve as both active sensory and communication signals. These EODs are maintained at steady frequencies of 200–600Hz throughout the lifespan, and thus represent a substantial metabolic investment. We investigated the effects of metabolic stress (food deprivation) on EOD amplitude (EODa) and EOD frequency (EODf) in E. virescens and found that only EODa decreases during food deprivation and recovers after restoration of feeding. Cortisol did not alter EODa under any conditions, and plasma cortisol levels were not changed by food deprivation. Both melanocortin hormones and social challenges caused transient EODa increases in both food-deprived and well-fed fish. Intramuscular injections of leptin increased EODa in food-deprived fish but not well-fed fish, identifying leptin as a novel regulator of EODa and suggesting that leptin mediates EODa responses to metabolic stress. The sensitivity of EODa to dietary energy availability likely arises because of the extreme energetic costs of EOD production in E. virescens and also could reflect reproductive strategies of iteroparous species that reduce social signaling and reproduction during periods of stress to later resume reproductive efforts when conditions improve.

Publisher URL: www.sciencedirect.com/science

DOI: S0018506X15000434