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Abstract Animals in nature seldom use their maximum performance abilities, likely in part due to context-dependent differences in performance motivation. Despite interest in the factors affecting performance expression, the physiological mechanisms underlying variation in performance motivation are poorly understood. We manipulated levels of the biogenic amine octopamine (OA) to test the hypothesis that OA drives motivation to express maximum bite force in male house crickets. We also tested the effect of antenna removal on bite force given prior evidence of potential links among antennaectomy, aggression, and OA. We found that administration of an OA antagonist, epinastine, significantly decreases realized maximum bite force, as does antenna removal. In addition, the performance decrement induced by antennaectomy is abolished by administration of excess OA, and that rescue effect is itself nullified by the simultaneous administration of epinastine. These data show that OA is an important mediator of performance in insects, and thus of performance motivation, and potentially a promising candidate for the short term manipulation of performance. 

Despite the conserved function of aggression across taxa in obtaining critical resources such as food and mates, serotonin’s (5-HT) modulatory role on aggressive behavior appears to be largely inhibitory for vertebrates but stimulatory for invertebrates. However, critical gaps exist in our knowledge of invertebrates that need to be addressed before definitively stating opposing roles for 5-HT and aggression. Specifically, the role of 5-HT receptor subtypes are largely unknown, as is the potential interactive role of 5-HT with other neurochemical systems known to play a critical role in aggression. Similarly, the influence of these systems in driving sex differences in aggressive behavior of invertebrates is not well understood. Here, we investigated these questions by employing complementary approaches in a novel invertebrate model of aggression, the stalk-eyed fly. A combination of altered social conditions, pharmacological manipulation and 5-HT2 receptor knockdown by siRNA revealed an inhibitory role of this receptor subtype on aggression. Additionally, we provide evidence for 5-HT2’s involvement in regulating neuropeptide F activity, a suspected inhibitor of aggression. However, this function appears to be stage-specific, altering only the initiation stage of aggressive conflicts. Alternatively, pharmacologically increasing systemic concentrations of 5-HT significantly elevated the expression of the neuropeptide tachykinin, which did not affect contest initiation but instead promoted escalation via production of high intensity aggressive behaviors. Notably, these effects were limited solely to males, with female aggression and neuropeptide expression remaining unaltered by any manipulation that affected 5-HT. Together, these results demonstrate a more nuanced role for 5-HT in modulating aggression in invertebrates, revealing an important interactive role with neuropeptides that is more reminiscent of vertebrates. The sex-differences described here also provide valuable insight into the evolutionary contexts of this complex behavior.