scholarly journals Sleep deprivation negatively impacts reproductive output in Drosophila melanogaster

2017 ◽  
Author(s):  
Sheetal Potdar ◽  
Danita K. Daniel ◽  
Femi A. Thomas ◽  
Shraddha Lall ◽  
Vasu Sheeba
Keyword(s):  
Sleep Deprivation ◽  
Dopaminergic Neurons ◽  
Reproductive Output ◽  
Negative Impact ◽  
Sleep Loss ◽  
Model Organisms ◽  
Loss Of Function ◽  
Mechanical Perturbation ◽  
Transient Activation ◽  
Sleep Deficit

AbstractMost animals sleep or exhibit a sleep-like state, yet the adaptive significance of this phenomenon remains unclear. Although reproductive deficits are associated with lifestyle induced sleep deficiencies, how sleep loss affects reproductive physiology is poorly understood, even in model organisms. We aimed to bridge this mechanistic gap by impairing sleep in female fruit flies and testing its effect on egg output. We find that sleep deprivation by feeding caffeine or by mechanical perturbation results in decreased egg output. Transient activation of wake-promoting dopaminergic neurons decreases egg output in addition to sleep levels, thus demonstrating a direct negative impact of sleep deficit on reproductive output. Similarly, loss-of-function mutation in dopamine transporter fumin (fmn)leads to both significant sleep loss and lowered fecundity. This demonstration of a direct relationship between sleep and reproductive fitness indicates a strong driving force for the evolution of sleep.

scholarly journals Residual, differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel
Keyword(s):  
Sleep Deprivation ◽  
Response Speed ◽  
Sleep Loss ◽  
Sleep Restriction ◽  
Total Sleep Deprivation ◽  
Psychomotor Vigilance Test ◽  
Recovery Sleep ◽  
Time In Bed ◽  
Neurobehavioral Deficits ◽  
Chronic Sleep

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.

scholarly journals Multiple Pathways of LRRK2-G2019S/Rab10 Interaction in Dopaminergic Neurons

2021 ◽  
pp. 1-16
Author(s):  
Alison Fellgett ◽  
C. Adam Middleton ◽  
Jack Munns ◽  
Chris Ugbode ◽  
David Jaciuch ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Genetic Interaction ◽  
In Vitro Assays ◽  
Rab Proteins ◽  
Circadian Activity ◽  
Loss Of Function ◽  
Lrrk2 G2019s

Background: Inherited mutations in the LRRK2 protein are the common causes of Parkinson’s disease, but the mechanisms by which increased kinase activity of mutant LRRK2 leads to pathological events remain to be determined. In vitro assays (heterologous cell culture, phospho-protein mass spectrometry) suggest that several Rab proteins might be directly phosphorylated by LRRK2-G2019S. An in vivo screen of Rab expression in dopaminergic neurons in young adult Drosophila demonstrated a strong genetic interaction between LRRK2-G2019S and Rab10. Objective: To determine if Rab10 is necessary for LRRK2-induced pathophysiological responses in the neurons that control movement, vision, circadian activity, and memory. These four systems were chosen because they are modulated by dopaminergic neurons in both humans and flies. Methods: LRRK2-G2019S was expressed in Drosophila dopaminergic neurons and the effects of Rab10 depletion on Proboscis Extension, retinal neurophysiology, circadian activity pattern (‘sleep’), and courtship memory determined in aged flies. Results: Rab10 loss-of-function rescued LRRK2-G2019S induced bradykinesia and retinal signaling deficits. Rab10 knock-down, however, did not rescue the marked sleep phenotype which results from dopaminergic LRRK2-G2019S. Courtship memory is not affected by LRRK2, but is markedly improved by Rab10 depletion. Anatomically, both LRRK2-G2019S and Rab10 are seen in the cytoplasm and at the synaptic endings of dopaminergic neurons. Conclusion: We conclude that, in Drosophila dopaminergic neurons, Rab10 is involved in some, but not all, LRRK2-induced behavioral deficits. Therefore, variations in Rab expression may contribute to susceptibility of different dopaminergic nuclei to neurodegeneration seen in people with Parkinson’s disease.

scholarly journals α-Synuclein-induced dysregulation of neuronal activity contributes to murine dopamine neuron vulnerability

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Abeer Dagra ◽  
Douglas R. Miller ◽  
Min Lin ◽  
Adithya Gopinath ◽  
Fatemeh Shaerzadeh ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neuronal Activity ◽  
Dopaminergic Neurons ◽  
Prolonged Exposure ◽  
D2 Receptor ◽  
Neuronal Firing ◽  
Dopamine Neurons ◽  
Loss Of Function ◽  
Therapeutic Implications

AbstractPathophysiological damages and loss of function of dopamine neurons precede their demise and contribute to the early phases of Parkinson’s disease. The presence of aberrant intracellular pathological inclusions of the protein α-synuclein within ventral midbrain dopaminergic neurons is one of the cardinal features of Parkinson’s disease. We employed molecular biology, electrophysiology, and live-cell imaging to investigate how excessive α-synuclein expression alters multiple characteristics of dopaminergic neuronal dynamics and dopamine transmission in cultured dopamine neurons conditionally expressing GCaMP6f. We found that overexpression of α-synuclein in mouse (male and female) dopaminergic neurons altered neuronal firing properties, calcium dynamics, dopamine release, protein expression, and morphology. Moreover, prolonged exposure to the D2 receptor agonist, quinpirole, rescues many of the alterations induced by α-synuclein overexpression. These studies demonstrate that α-synuclein dysregulation of neuronal activity contributes to the vulnerability of dopaminergic neurons and that modulation of D2 receptor activity can ameliorate the pathophysiology. These findings provide mechanistic insights into the insidious changes in dopaminergic neuronal activity and neuronal loss that characterize Parkinson’s disease progression with significant therapeutic implications.

121 Behavioral Attention Relationships Vary Between Demographic Groups Across Sleep Loss and Recovery

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A49-A50
Author(s):  
Caroline Antler ◽  
Erika Yamazaki ◽  
Tess Brieva ◽  
Courtney Casale ◽  
Namni Goel
Keyword(s):  
Sleep Deprivation ◽  
Repeated Measures ◽  
Age Groups ◽  
Response Speed ◽  
Sleep Loss ◽  
Demographic Groups ◽  
Time In Bed ◽  
Median Split ◽  
The Relationship ◽  
High Bmi

Abstract Introduction The Psychomotor Vigilance Test (PVT) is a behavioral attention measure widely used to describe sleep loss deficits. Although there are reported differences in PVT performance for various demographic groups, no study has examined the relationship between measures on the 10-minute PVT (PVT10) and the 3-minute PVT (PVT3) within sex, age, and body mass index (BMI) groups throughout a highly controlled sleep deprivation study. Methods Forty-one healthy adults (mean±SD ages, 33.9±8.9y) participated in a 13-night experiment [2 baseline nights (10h-12h time in bed, TIB) followed by 5 sleep restriction (SR1-5) nights (4h TIB), 4 recovery nights (R1-R4; 12h TIB), and 36h total sleep deprivation (TSD)]. A neurobehavioral test battery, including the PVT10 and PVT3 was completed every 2h during wakefulness. Repeated measures correlation (rmcorr) compared PVT10 and PVT3 lapses (reaction time [RT] >355ms [PVT3] and >500ms [PVT10]) and response speed (1/RT) by examining correlations by day (e.g., baseline day 2) and time point (e.g., 1000h-2000h) within sex groups (18 females), within age groups defined by a median split (median=32, range=21-49y), and within BMI groups defined by a median split (median=25, range=17-31). Results PVT10 and PVT3 1/RT was significantly correlated at all study days and time points excluding at baseline for the younger group and at R2 for the higher BMI group. PVT10 and PVT3 lapses showed overall lower correlations across the study relative to 1/RT. Lapses were not significantly correlated at baseline for any group, for males across recovery (R1-R4), for the high BMI group at R2-R4, for the older group at R2-R3, or for the younger group at SR5 or R3. Conclusion Differentiating participants based on age, sex, or BMI revealed important variation in the relationship between PVT10 and PVT3 measures across the study. Surprisingly, lapses were not significantly correlated at baseline for any demographic group or across recovery for males or the high BMI or older group. Thus, PVT10 and PVT3 lapses may be less comparable in certain populations when well-rested. These findings add to a growing literature suggesting demographic factors may be important factors to consider when evaluating the effects of sleep loss. Support (if any) ONR Award N00014-11-1-0361;NIH UL1TR000003;NASA NNX14AN49G and 80NSSC20K0243; NIHR01DK117488

293 Predictive utility of a brief scale to identify U.S. Army Soldiers who are genetically vulnerable and resilient to sleep loss

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A117-A117
Author(s):  
Janna Mantua ◽  
Carolyn Mickelson ◽  
Jacob Naylor ◽  
Bradley Ritland ◽  
Alexxa Bessey ◽  
...  
Keyword(s):  
Decision Making ◽  
Reaction Time ◽  
Sleep Deprivation ◽  
Cognitive Performance ◽  
Response Inhibition ◽  
Sleep Loss ◽  
Cutoff Score ◽  
Cognitive Subscale ◽  
Army Soldiers ◽  
Psychomotor Vigilance

Abstract Introduction Sleep loss that is inherent to military operations can lead to cognitive errors and potential mission failure. Single Nucleotide Polymorphisms (SNPs) allele variations of several genes (COMT, ADORA2A, TNFa, CLOCK, DAT1) have been linked with inter-individual cognitive resilience to sleep loss through various mechanisms. U.S. Army Soldiers with resilience-related alleles may be better-suited to perform cognitively-arduous duties under conditions of sleep loss than those without these alleles. However, military-wide genetic screening is costly, arduous, and infeasible. This study tested whether a brief survey of subjective resilience to sleep loss (1) can demarcate soldiers with and without resilience-related alleles, and, if so, (2) can predict cognitive performance under conditions of sleep loss. Methods Six SNPs from the aforementioned genes were sequenced from 75 male U.S. Army special operations Soldiers (age 25.7±4.1). Psychomotor vigilance, response inhibition, and decision-making were tested after a night of mission-driven total sleep deprivation. The Iowa Resilience to Sleeplessness Test (iREST) Cognitive Subscale, which measures subjective cognitive resilience to sleep loss, was administered after a week of recovery sleep. A receiver operating characteristic (ROC) curve was used to determine whether the iREST Cognitive Subscale can discriminate between gene carriers, and a cutoff score was determined. Cognitive performance after sleep deprivation was compared between those below/above the cutoff score using t-tests or Mann-Whitney U tests. Results The iREST discriminated between allele variations for COMT (ROC=.65,SE=.07,p=.03), with an optimal cutoff score of 3.03 out of 5, with 90% sensitivity and 51.4% specificity. Soldiers below the cutoff score had significantly poorer for psychomotor vigilance reaction time (t=-2.39,p=.02), response inhibition errors of commission (U=155.00,W=246.00,p=.04), and decision-making reaction time (t=2.13,p=.04) than Soldiers above the cutoff score. Conclusion The iREST Cognitive Subscale can discriminate between those with and without specific vulnerability/resilience-related genotypes. If these findings are replicated, the iREST Cognitive Subscale could be used to help military leaders make decisions about proper personnel placement when sleep loss is unavoidable. This would likely result in increased safety and improved performance during military missions. Support (if any) Support for this study came from the Military Operational Medicine Research Program of the United States Army Medical Research and Development Command.

scholarly journals POS0998 SPONDYLOARTHRITIS AND SLEEP DISORDERS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 767.2-768
Author(s):  
S. Lahrichi ◽  
K. Nassar ◽  
S. Janani
Keyword(s):  
Functional Impairment ◽  
Sleep Disturbances ◽  
Negative Impact ◽  
University Hospital ◽  
Quality Of Sleep ◽  
The Mean ◽  
Sleep Deficit ◽  
Impaired Sleep ◽  
The Impact

Background:Spondyloarthropathies (SpA) are a group of chronic and progressive diseases, characterized in particular by a progressive stiffening of the spine, spreading to neighboring joints or to certain tissues, which could lead in the long term to progressive stiffening and functional impairment. This conditioncancauseinsomnia problems and impaired sleep quality.Objectives:To assess the impact of SpA on the quality of sleep.Methods:This is a retrospective study over a period of 4 years from January 2015 to December 2019, including all the medical records of patients with SpA followed in the Department of Rheumatology of the University Hospital of Ibn Rochd, Casablanca. We evaluated for each patient two validated scores: the Epworth somnolence scale rated from 0 to 24, and the Pittsburgh sleep score rated from 0 to 21 with 7 components. Patients with a psychiatric history or who were followed up for neurological pathologies were excluded.Results:178 patients were included. 60.67% were men with an average age of 36.32 years (14-68 years). 45.01% had axial SpA, 29.77% had psoriatic arthritis, and 25.22% were followed for SpA associated with inflammatory bowel disease. 45% had associated comorbidities: there were 18 diabetics and 34 hypertensive, 16.58% were smokers. Clinically, 85.42% presented a back pain initially on examination, 55% presented a polyarthralgia, and 39.88% an oligoarthritis. 63% had radiological sacroiliitis, and 35.14% had bilateral coxitis. 13.48% had a positive HLA B27 and 58.89% had a positive inflammatory assessment with very high activity indices,with a mean of 4.6. 64.66% of the patients received NSAIDs,of which 11% responded well. 57% were treated with csDMARDs, and 17.86% were treated with biologics. At the time of our study, the mean visual analog scale was 5.84 ± 1.7 out of 10 (2-9). The mean Epworth score was 8.38 ± 5.2 (0-21). 56.1% of patients had no sleep debt, 33.3% had a sleep deficit, and only 10.6% had signs of drowsiness. For the overall Pittsburgh score, the mean was 7.02 ± 3.6 (1-18). The mean of “subjective quality of sleep” was 1.12, “sleep latency” was 1.22, “duration of sleep” was 1.06, “usual sleep efficiency” was 0.74, “Sleep disturbance” of 1.28, “use of a sleep medication” of 0.54, and the average of the component concerning “poor shape during the day” was 1.03 out of 3. The LEQUESNE index went from an average of 6 to 8, which corresponds to an average handicap (P = 0.2) over a period of 3 years. 68% of the patients had an alteration in the quality of sleep, starting on average three years after the onset of symptoms. 11% reported having experiencedanxiety and depressive symptoms, and reported having used antidepressants or anxiolytics in the past 5 years.Conclusion:Our study showed the negative impact of SpA on the duration and overall quality of sleep. The degree of pain as well as functional impairment can cause and worsen sleep disturbances in SpA. We have shown that the Pittsburg score increases significantly with the increase of pain.The Lequesne score and that the Epworth score increase with disease activity[1].References:[1]StolwijkC,vanTubergenA,Castillo-OrtizJD,BoonenA.Prevalenceofextra-articularmanifestationsinpatientswithankylosingspondylitis:asystematicreviewandmeta-analysis.AnnRheumDis2015;74:65—73.Disclosure of Interests:None declared.

137 Recovery Dynamics in a Biomathematical Model of Fatigue

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A56-A56
Author(s):  
Mark McCauley ◽  
Peter McCauley ◽  
Hans Van Dongen
Keyword(s):  
Sleep Deprivation ◽  
Goodness Of Fit ◽  
Sleep Loss ◽  
Sleep Restriction ◽  
Commercial Aviation ◽  
Circadian Misalignment ◽  
Total Sleep Deprivation ◽  
Homeostatic Process ◽  
Recovery Sleep

Abstract Introduction In commercial aviation and other operational settings where biomathematical models of fatigue are used for fatigue risk management, accurate prediction of recovery during rest periods following duty periods with sleep loss and/or circadian misalignment is critical. The recuperative potential of recovery sleep is influenced by a variety of factors, including long-term, allostatic effects of prior sleep/wake history. For example, recovery tends to be slower after sustained sleep restriction versus acute total sleep deprivation. Capturing such dynamics has proven to be challenging. Methods Here we focus on the dynamic biomathematical model of McCauley et al. (2013). In addition to a circadian process, this model features differential equations for sleep/wake regulation including a short-term sleep homeostatic process capturing change in the order of hours/days and a long-term allostatic process capturing change in the order of days/weeks. The allostatic process modulates the dynamics of the homeostatic process by shifting its equilibrium setpoint, which addresses recently observed phenomena such as reduced vulnerability to sleep loss after banking sleep. It also differentiates the build-up and recovery rates of fatigue under conditions of chronic sleep restriction versus acute total sleep deprivation; nonetheless, it does not accurately predict the disproportionately rapid recovery seen after total sleep deprivation. To improve the model, we hypothesized that the homeostatic process may also modulate the allostatic process, with the magnitude of this effect scaling as a function of time awake. Results To test our hypothesis, we added a parameter to the model to capture modulation by the homeostatic process of the allostatic process build-up during wakefulness and dissipation during sleep. Parameter estimation using previously published laboratory datasets of fatigue showed this parameter as significantly different from zero (p<0.05) and yielding a 10%–20% improvement in goodness-of-fit for recovery without adversely affecting goodness-of-fit for pre-recovery days. Conclusion Inclusion of a modulation effect of the allostatic process by the homeostatic process improved prediction accuracy in a variety of sleep loss and circadian misalignment scenarios. In addition to operational relevance for duty/rest scheduling, this finding has implications for understanding mechanisms underlying the homeostatic and allostatic processes of sleep/wake regulation. Support (if any) Federal Express Corporation

scholarly journals Targeting hydroxycinnamoyl CoA: shikimate hydroxycinnamoyl transferase for lignin modification in Brachypodium distachyon

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Juan Carlos Serrani-Yarce ◽  
Luis Escamilla-Trevino ◽  
Jaime Barros ◽  
Lina Gallego-Giraldo ◽  
Yunqiao Pu ◽  
...  
Keyword(s):  
Negative Impact ◽  
Lignin Content ◽  
Brachypodium Distachyon ◽  
Lignin Biosynthesis ◽  
Reverse Direction ◽  
Wall Structure ◽  
Kinetic Properties ◽  
Loss Of Function ◽  
Down Regulation ◽  
Lignin Modification

Abstract Background Hydroxycinnamoyl CoA: shikimate hydroxycinnamoyl transferase (HCT) is a central enzyme of the so-called “esters” pathway to monolignols. As originally envisioned, HCT functions twice in this pathway, to form coumaroyl shikimate and then, in the “reverse” direction, to convert caffeoyl shikimate to caffeoyl CoA. The discovery of a caffeoyl shikimate esterase (CSE) that forms caffeic acid directly from caffeoyl shikimate calls into question the need for the reverse HCT reaction in lignin biosynthesis. Loss of function of HCT gives severe growth phenotypes in several dicot plants, but less so in some monocots, questioning whether this enzyme, and therefore the shikimate shunt, plays the same role in both monocots and dicots. The model grass Brachypodium distachyon has two HCT genes, but lacks a classical CSE gene. This study was therefore conducted to evaluate the utility of HCT as a target for lignin modification in a species with an “incomplete” shikimate shunt. Results The kinetic properties of recombinant B. distachyon HCTs were compared with those from Arabidopsis thaliana, Medicago truncatula, and Panicum virgatum (switchgrass) for both the forward and reverse reactions. Along with two M. truncatula HCTs, B. distachyon HCT2 had the least kinetically unfavorable reverse HCT reaction, and this enzyme is induced when HCT1 is down-regulated. Down regulation of B. distachyon HCT1, or co-down-regulation of HCT1 and HCT2, by RNA interference led to reduced lignin levels, with only modest changes in lignin composition and molecular weight. Conclusions Down-regulation of HCT1, or co-down-regulation of both HCT genes, in B. distachyon results in less extensive changes in lignin content/composition and cell wall structure than observed following HCT down-regulation in dicots, with little negative impact on biomass yield. Nevertheless, HCT down-regulation leads to significant improvements in biomass saccharification efficiency, making this gene a preferred target for biotechnological improvement of grasses for bioprocessing.

scholarly journals CaM kinase IIδ2-dependent regulation of vascular smooth muscle cell polarization and migration

2008 ◽  
Vol 294 (6) ◽  
pp. C1465-C1475 ◽  
Author(s):  
Melissa Z. Mercure ◽  
Roman Ginnan ◽  
Harold A. Singer
Keyword(s):  
Smooth Muscle ◽  
Cell Migration ◽  
Vascular Smooth Muscle ◽  
Cell Monolayer ◽  
Leading Edge ◽  
Cell Polarization ◽  
Loss Of Function ◽  
Downstream Signaling ◽  
Transient Activation ◽  
And Migration

Previous studies indicate involvement of the multifunctional Ca2+/calmodulin-dependent protein kinase II (CaMKII) in vascular smooth muscle (VSM) cell migration. In the present study, molecular loss-of-function studies were used specifically to assess the role of the predominant CaMKIIδ2 isoform on VSM cell migration using a scratch wound healing assay. Targeted CaMKIIδ2 knockdown using siRNA or inhibition of activity by overexpressing a kinase-negative mutant resulted in attenuation of VSM cell migration. Temporal and spatial assessments of kinase autophosphorylation indicated rapid and transient activation in response to wounding, in addition to a sustained activation in the leading edge of migrating and spreading cells. Furthermore, siRNA-mediated suppression of CaMKIIδ2 resulted in the inhibition of wound-induced Rac activation and Golgi reorganization, and disruption of leading edge morphology, indicating an important function for CaMKIIδ2 in regulating VSM cell polarization. Numerous previous reports link activation of CaMKII to ERK1/2 signaling in VSM. Wound-induced ERK1/2 activation was also found to be dependent on CaMKII; however, ERK activity did not account for effects of CaMKII in regulating Golgi polarization, indicating alternative mechanisms by which CaMKII affects the complex events involved in cell migration. Wounding a VSM cell monolayer results in CaMKIIδ2 activation, which positively regulates VSM cell polarization and downstream signaling, including Rac and ERK1/2 activation, leading to cell migration.

scholarly journals Modulation of sleep-courtship balance by nutritional status in Drosophila

2020 ◽  
Author(s):  
José M. Duhart ◽  
Victoria Baccini ◽  
Yanan Zhang ◽  
Daniel R. Machado ◽  
Kyunghee Koh
Keyword(s):  
Nutritional Status ◽  
Calcium Imaging ◽  
Dopaminergic Neurons ◽  
Potential Benefit ◽  
Sleep Loss ◽  
Female Partners ◽  
Sleep Drive ◽  
Protocerebral Bridge ◽  
The Cost ◽  
Nighttime Sleep

AbstractSleep is essential but incompatible with other behaviors, and thus sleep drive competes with other motivations. We previously showed Drosophila males balance sleep and courtship via octopaminergic neurons that act upstream of courtship-regulating P1 neurons (Machado et al., 2017). Here we show nutrition modulates the sleep-courtship balance and identify sleep-regulatory neurons downstream of P1 neurons. Yeast-deprived males exhibited attenuated female-induced nighttime sleep loss yet normal daytime courtship, which suggests male flies consider nutritional status in deciding whether the potential benefit of pursuing female partners outweighs the cost of losing sleep. Trans-synaptic tracing and calcium imaging identified dopaminergic neurons projecting to the protocerebral bridge (DA-PB) as postsynaptic partners of P1 neurons. Activation of DA-PB neurons led to reduced sleep in normally fed but not yeast-deprived males. Additional PB-projecting neurons regulated male sleep, suggesting several groups of PB-projecting neurons act downstream of P1 neurons to mediate nutritional modulation of the sleep-courtship balance.

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