Abstract
Neuromodulators such as monoamines are often expressed in neurons that also release at least one fast-acting neurotransmitter. The release of a combination of transmitters provides both “classical” and “modulatory” signals that could produce diverse and/or complementary effects in associated circuits. Here, we establish that the majority of Drosophila octopamine (OA) neurons are also glutamatergic and identify the individual contributions of each neurotransmitter on sex-specific behaviors. Males without OA display low levels of aggression and high levels of inter-male courtship. Males deficient for dVGLUT solely in OA-glutamate neurons (OGNs) also exhibit a reduction in aggression, but without a concurrent increase in inter-male courtship. Within OGNs, a portion of VMAT and dVGLUT puncta differ in localization suggesting spatial differences in OA signaling. Our findings establish a previously undetermined role for dVGLUT in OA neurons and suggests that glutamate uncouples aggression from OA-dependent courtship-related behavior. These results indicate that dual neurotransmission can increase the efficacy of individual neurotransmitters while maintaining unique functions within a multi-functional social behavior neuronal network.
Highlights
The classical view of information transfer for many decades was that each neuron released a single neurotransmitter, leading to the ‘one neuron, one transmitter’ hypothesis [1], formalized by John Eccles as Dale’s Principle [2]
We ask how does the release of more than one neurotransmitter from a single neuron impact circuits that control behavior? We determined the monoamine octopamine and the classical transmitter glutamate are co-expressed in the Drosophila adult CNS
We focused on OA neurons that co-express dVGLUT (OA-glutamate neurons (OGNs))
Summary
The classical view of information transfer for many decades was that each neuron released a single neurotransmitter, leading to the ‘one neuron, one transmitter’ hypothesis [1], formalized by John Eccles as Dale’s Principle [2]. The release of two neurotransmitters could impact information transfer by several mechanisms that are not mutually exclusive including; attenuating signals by modulating presynaptic autoreceptors, transmitting spatially distinct signals by segregating specific vesicle populations to different axon terminals, or conveying similar information through the release of both neurotransmitters from the same synaptic vesicle [8,9,10,11]. At post-synaptic targets, the release of two transmitters can enhance the strength of the same signal and/or convey unique signals through spatially-restricted receptor expression and second messenger cascades [7, 14]. While recent studies have provided insight into these phenomena at the cellular level [11, 12, 15, 16], the behavioral relevance of co-transmission in normal as well as pathological conditions is an area of considerable complexity and interest
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