Characterization of Drosophila octopamine receptor neuronal expression using MiMIC‐converted Gal4 lines
Octopamine, the invertebrate analog of norepinephrine, is known to modulate a large variety of behaviors in Drosophila including feeding initiation, locomotion, aggression, and courtship, among many others. Significantly less is known about the identity of the neurons that receive octopamine input a...
Gespeichert in:
Veröffentlicht in: | Journal of comparative neurology (1911) 2020-09, Vol.528 (13), p.2174-2194 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Octopamine, the invertebrate analog of norepinephrine, is known to modulate a large variety of behaviors in Drosophila including feeding initiation, locomotion, aggression, and courtship, among many others. Significantly less is known about the identity of the neurons that receive octopamine input and how they mediate octopamine‐regulated behaviors. Here, we characterize adult neuronal expression of MiMIC‐converted Trojan‐Gal4 lines for each of the five Drosophila octopamine receptors. Broad neuronal expression was observed for all five octopamine receptors, yet distinct differences among them were also apparent. Use of immunostaining for the octopamine neurotransmitter synthesis enzyme Tdc2, along with a novel genome‐edited conditional Tdc2‐LexA driver, revealed all five octopamine receptors express in Tdc2/octopamine neurons to varying degrees. This suggests autoreception may be an important circuit mechanism by which octopamine modulates behavior.
New octopamine receptor MiMIC‐Gal4 lines, in conjunction with B3RT‐Tdc2‐LexA intersectional genetics, reveal potential neuronal octopamine autoreceptor locations in Drosophila melanogaster. This intersectional genetic tool can be further utilized to identify the subset of Tdc2‐expressing neurons within any Gal4 driver of interest. |
---|---|
ISSN: | 0021-9967 1096-9861 |
DOI: | 10.1002/cne.24883 |