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The title of the study is "Flight initiation and maintenance deficits in flies with genetically altered biogenic amine levels". It shows that in contrast to what was believed for about 20 years, octopamine is not required for flight initiation nor maintenance. Instead, we uncovered antagonistic interplay between octopamine and its synthesis precurser tyramine. This study was done using flies mutant for the enzyme (tyramine beta hydroxylase) catalyzing the synthesis of octopamine from tyramine. These flies lack octopamine completely and sport 8-fold increased tyramine levels. Reducing the action of tyramine alone by feeding tyramine receptor blockers to these flies is sufficient to restore flight performance to the otherwise severely impaired mutants. However, also restoring octopamine alone rescues the mutant defect. Further experiments suggest that octopamine and tyramine exert their antagonistic effects probably at different locations in the fly's nervous system.
This study was important for my own research as octopamine is regarded as the main transmitter mediating reward and I study learning in flying flies (it means I can't use these mutants in my learning paradigm
, at least not without restricting the mutation only to certain neurons - work in progress). Another point worth noting is the interesting parallel of the main transmitter of reward in flies (octopamine) controlling behavior, just as the main mediator of reward in humans (dopamine) also controls behavior (as evidenced in Parkinson's patients lacking dopaminergic neurons).Personally for me, this publication comes at a crucial time when I'm actively on the hunt for a faculty position. A paper in this journal is significant, because of its impact factor (IF) of about 7.5 (Explanation of IF).
An entertaining side note to this is that at least one of my evaluators at the DFG did not spot the obvious connection of this work to my research focus and suggested I dropped this project...
Posted on Monday 20 August 2007 - 14:33:11 comment: 0
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