Journal
CURRENT BIOLOGY
Volume 19, Issue 14, Pages 1206-1209Publisher
CELL PRESS
DOI: 10.1016/j.cub.2009.05.051
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Funding
- Royal Society of New Zealand Marsden Fund [UOO312, UOO0615]
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Queen mandibular pheromone (QMP) is produced by honey bee queens and used to regulate the behavior and physiology of their nestmates [1]. QMP has recently been shown to block aversive learning in young worker bees, an effect that can be mimicked by treating bees with one of QMP's key components, homovanillyl alcohol (HVA) [2]. Although the mechanisms underlying this blockade remain unclear, HVA has been found to lower brain dopamine levels and to alter intracellular levels of cAMP in brain centers involved in learning and memory [3]. These findings led to the hypothesis that HVA targets dopamine pathways in the brain [3], which are known to play a critical role in the formation of aversive olfactory memories [4-8]. Here, we investigate the possibility that HVA interacts directly with dopamine receptors in the bee. We show that HVA selectively activates the D2-like dopamine receptor AmDOP3 but has neither agonist nor antagonist activity on the D1-like receptors AmDOP1 or AmDOP2 nor agonist activity on the octopamine receptor AmOA1. These results suggest a direct molecular mechanism by which queen pheromone can modulate dopamine signaling pathways. They also implicate the dopamine receptor AmDOP3 in HVA-induced blockade of aversive learning in young worker bees.
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