Identified Serotonin-Releasing Neurons Induce Behavioral Quiescence and Suppress Mating inDrosophila

Abstract

Animals show different levels of activity that are reflected in sensory responsiveness and endogenously generated behaviors. Biogenic amines have been determined to be causal factors for these states of arousal. It is well established that, in Drosophila, dopamine and octopamine promote increased arousal. However, little is known about factors that regulate arousal negatively and induce states of quiescence. Moreover, it remains unclear whether global, diffuse modulatory systems comprehensively affecting brain activity determine general states of arousal. Alternatively, individual aminergic neurons might selectively modulate the animals' activity in a distinct behavioral context. Here, we show that artificially activating large populations of serotonin-releasing neurons induces behavioral quiescence and inhibits feeding and mating. We systematically narrowed down a role of serotonin in inhibiting endogenously generated locomotor activity to neurons located in the posterior medial protocerebrum. We identified neurons of this cell cluster that suppress mating, but not feeding behavior. These results suggest that serotonin does not uniformly act as global, negative modulator of general arousal. Rather, distinct serotoninergic neurons can act as inhibitory modulators of specific behaviors.

Serotonergic neuronal death and concomitant serotonin deficiency curb copulation ability of Drosophila platonic mutants

“…24) in the brain trigger copulation behaviour5. Also, there is evidence of the involvement of the brain serotonergic system in regulating motivation to copulate2526. These brain neurons appear to turn ON and OFF, via as yet unidentified descending neurons, the VNC motor centre for the control of copulation, whose development and function are likely regulated by the Trh-GAL4 -positive dsx neurons we found in this study.…”

Drosophila Clock Is Required in Brain Pacemaker Neurons to Prevent Premature Locomotor Aging Independently of Its Circadian Function

“…That loss, like the accelerated ARLI phenotype (Fig 3A), was rescued by Clk expression restricted to the PDF neurons (S10A Fig). In contrast, the size of several serotonergic clusters in a broad dorso-lateral protocerebral region [see [37]], where the PPL1 is located, did not differ between aging Clk AR and control flies (S11 Fig). Accelerated ARLI due to impaired Clk function appears thus selectively associated with a loss of TH-IR neurons in the PPL1 cluster, although we cannot rule out that a few PAM neurons are also affected (see also below).…”

“…(A) Bars display the mean ± SEM of TH-IR (PPL1) and 5-HT-IR (PLP, LP and ALP) cell numbers, from 8–10 brain hemispheres per genotype. ALP: Anterior Lateral Protocerebrum, LP: Lateral Protocerebrum, PLP: Posterior Lateral Protocerebrum [37]. (B) z-projections of the anterior and posterior parts of a representative 31-day-old Clk AR brain, double-labeled with anti-TH and anti-5-HT antibodies, as indicated.…”

Unraveling the Evolutionary Determinants of Sleep

“…Moreover, when these systems have been manipulated pharmacologically or genetically in zebrafish, they have been shown to regulate arousal in much the same way as they do in mammals (Figure 2) [163–167]. Similarly, in flies, activation of aminergic and cholinergic neurons promotes arousal, though some serotonergic neurons may suppress it [28, 168–170]. As in mammals and zebrafish, GABAergic neurons also suppress arousal in flies [117, 127, 128].…”