Profound flight performance deficit in Drosophila lacking octopamine
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CONTRIBUTORS:
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CONFERENCE NAME:
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CONF. LOCATION:
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Viene, Austria
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CONFERENCE YEAR:
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2006
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PUB TYPE:
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Conference Presentation
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SUBJECT(S):
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Neuroscience, neurobiology, metabolism, insect flight
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DISCIPLINE:
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Biology
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HTTP:
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LANGUAGE:
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English
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PUB ID:
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103-426-006
(Last edited on
2006/04/13 03:56:48 GMT-6)
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SPONSOR(S):
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ABSTRACT:
Insect flight is one of the fastest, most intense and most energy-demanding motor behaviors. At 1 m per second and up to 350Hz wing beat frequency flies perform highly coordinated steering maneuvers, and ATP turnover rates may increase more than 100 fold over rest. This athlete motor behavior is modulated on multiple levels by the biogenic amine, octopamine. Within the CNS octopamine can directly switch on the flight central pattern generator and it may affect the motivation to fly. In the periphery, octopamine sensitizes wing hinge receptors and alters muscle contraction kinetics. In locusts, octopamine released from central neurons directly onto wing power muscles enhances muscle glycolysis, poising them metabolically for take-off. During prolonged flight, locust flight muscles are fueled by lipids, due to inhibition of octopaminergic neurons. In contrast, Dipteran flight muscles rely exclusively on carbohydrate metabolisms. This study addresses the role for octopamine in dipteran flight behavior by genetic manipulation in Drosophila.
We find that flies lacking octopamine (Tbh, tyramine-beta-hydroxylase null mutants) show a profound flight performance deficit in both spontaneous and stimulated flight compared to wildtype controls. Four lines of evidence suggest that neither the ability to fly nor the development of the flight machinery is impaired in Tbh mutants: (i) wing beat frequencies, (ii) wing beat amplitudes, (iii) flight muscle structure (length of myofibrils), and (iv) the number and dendritic structure of flight motoneurons are unaffected in Tbh mutants. Furthermore, the flight phenotype is partially rescued by supplementing octopamine throughout development. These results underscore the physiological rather than developmental role of octopamine in flight performance. Results of genetic rescues will also be presented. Shorter flight durations in flies lacking octopamine could either be caused by a decreased motivation to fly, or by increased fatigue in Tbh mutants, or by a combination of both. The results of two additional, ongoing lines of experiments will be presented to elucidate the physiological cause for the Tbh phenotype. First, immunohistochemistry determines whether the behavioral rescue is due to restitution of octopamine in the CNS or in the periphery. Second, glycolytic rates are measured in mutant, wildtype and rescued muscles.
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