Premium
Drosophila mutants lacking octopamine exhibit impairment in aversive olfactory associative learning
Author(s) -
Iliadi Konstantin G.,
Iliadi Natalia,
Boulianne Gabrielle L.
Publication year - 2017
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.13654
Subject(s) - octopamine (neurotransmitter) , associative learning , neuroscience , biology , olfaction , olfactory memory , mutant , mushroom bodies , neurotransmitter , insect , olfactory system , drosophila melanogaster , genetics , olfactory bulb , central nervous system , receptor , gene , serotonin , ecology
Octopamine is a biogenic amine in invertebrates that is considered a functional homolog of vertebrate norepinephrine, acting as a neurotransmitter, neuromodulator and neurohormone. Octopamine regulates many physiological processes such as metabolism, reproduction and different types of behaviour including learning and memory. Previous studies in insects led to the notion that acquisition of an olfactory memory depends on the octopaminergic system during appetitive (reward‐based) learning, but not in the case of aversive (punishment‐based) learning. Here, we provide several lines of evidence demonstrating that aversive associative olfactory learning in Drosophila is also dependent on octopamine signalling. Specifically, we used Drosophila Tβh (tyramine‐β‐hydroxylase) mutants, which lack octopamine and are female sterile, to determine whether octopamine plays a role in aversive learning. We show that Tβh mutant flies exhibit a significant reduction in learning compared to control lines that is independent of either genetic background or the methods used to induce aversive olfactory memory. We also show that the learning deficits observed in Tβh mutants are not due to defects in sensorimotor behaviours. Finally, to unambiguously demonstrate that octopamine synthesis plays a role in aversive olfactory learning, we performed rescue experiments using the Gal4/ UAS system. We show that expression of UAS ‐ Tβh in octopamine/tyraminergic neurons using Tdc2‐Gal4 in Tβh null mutant flies fully rescued both the aversive learning defects and female sterility observed in Tβh mutants.