Female contact modulates male aggression via a sexually dimorphic GABAergic circuit in Drosophila.
Intraspecific male-male aggression, which is important for sexual selection, is regulated by environment, experience and internal states through largely undefined molecular and cellular mechanisms. To understand the basic neural pathway underlying the modulation of this innate behavior, we established a behavioral assay in Drosophila melanogaster and investigated the relationship between sexual experience and aggression. In the presence of mating partners, adult male flies exhibited elevated levels of aggression, which was largely suppressed by prior exposure to females via a sexually dimorphic neural mechanism. The suppression involved the ability of male flies to detect females by contact chemosensation through the pheromone-sensing ion channel ppk29 and was mediated by male-specific GABAergic neurons acting on the GABAA receptor RDL in target cells. Silencing or activating this circuit led to dis-inhibition or elimination of sex-related aggression, respectively. We propose that the GABAergic inhibition represents a critical cellular mechanism that enables prior experience to modulate aggression.
1] Department of Physiology and Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, California, USA. [2] [3].
Quan
Q
Yuan
1] Department of Physiology and Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, California, USA. [2].
Yuanquan
Y
Song
1] Department of Physiology and Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, California, USA. [2].
Chung-Hui
CH
Yang
Department of Physiology and Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, California, USA.
Lily Yeh
LY
Jan
1] Department of Physiology and Howard Hughes Medical Institute, University of California at San Francisco, San Francisco, California, USA. [2].
Yuh Nung
YN
Jan
D006916:5-Hydroxytryptophan / Q000494:pharmacology; D000374:Aggression / Q000502:physiology*; D000704:Analysis of Variance; D000818:Animals; D030801:Animals, Genetically Modified; D001921:Brain / Q000166:cytology*; D016827:CD8 Antigens / Q000378:metabolism; D004330:Drosophila; D029721:Drosophila Proteins / Q000235:genetics; D005260:Female; D059330:GABAergic Neurons / Q000502:physiology*; D005968:Glutamate Decarboxylase / Q000378:metabolism; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D007473:Ion Channels / Q000235:genetics; D008297:Male; D009415:Nerve Net / Q000378:metabolism; D009433:Neural Inhibition / Q000502:physiology; D034622:RNA Interference / Q000502:physiology; D044302:Receptor, Serotonin, 5-HT1B / Q000235:genetics / Q000378:metabolism; D011963:Receptors, GABA-A / Q000235:genetics / Q000378:metabolism; D012727:Sex Characteristics; D012726:Sexual Behavior, Animal / Q000502:physiology*; D013697:Thermosensing / Q000502:physiology; D050495:Vesicular Inhibitory Amino Acid Transport Proteins / Q000378:metabolism
D016827:CD8 Antigens; D029721:Drosophila Proteins; D007473:Ion Channels; C573946:PPK29 protein, Drosophila; D044302:Receptor, Serotonin, 5-HT1B; D011963:Receptors, GABA-A; D050495:Vesicular Inhibitory Amino Acid Transport Proteins; C493406:vesicular GABA transporter; D049452:Green Fluorescent Proteins; D006916:5-Hydroxytryptophan; D005968:Glutamate Decarboxylase