Science and Nanotechnology of Superhard Materials

Genetic intersectional strategies were employed to exclude GABAergic neurons from the 5HT-1B+/fru+ neurons. Either silencing or activating 5HT-1B+/ fru+/GAD− neurons did not produce disinhibition or aggression phenotype. These results suggest that perhaps only the 5-HT1B+/fru+/GAD+ triple positive neurons are essential for suppressing male–male aggression by female contact. Finally, the authors discovered that type A GABA receptor, Resistant to dieldrin (RDL), was involved in inhibiting aggression by prior female contact. Acute activation of the RDL+/fru+ neurons increased male–male aggression, indicating an aggression-promoting role of these RDL+/fru+ neurons. Taken together, these results suggest that GABAergic 5HT-1B+/fru+ neurons suppress male aggression by inhibiting downstream RDL+/fru+ neurons. It would be interesting to directly label and manipulate those GABAergic 5HT1B+/fru+ neurons and examine the behavioral consequences. This study opens a new avenue to explore how sexual experience modulates aggressive behavior and identifies a set of neural circuits involved in this process. It remains to be elucidated how pheromone signals were relayed from ppk29 neurons to those GABAergic 5HT-1B+/fru+ neurons. For example, are those GABAergic 5HT-1B+/fru+ neurons sensitive to female pheromones? The downstream RDL+ neurons remain to be clearly defined and the functional connectivity between the GABAergic 5HT-1B+/fru+ neurons and RDL+ neurons needs to be characterized. Most interestingly, what is the neural mechanism underlying the temporal transition from promoting aggression by acute female contact to inhibiting aggression by chronic female contact? An understanding of the neural circuits that mediate social modulation on aggression in flies may shed insights into the neural basis of human violence.