scholarly journals Protocerebral Bridge Neurons That Regulate Sleep in Drosophila melanogaster

2021 ◽  
Vol 15 ◽  
Author(s):  
Jun Tomita ◽  
Gosuke Ban ◽  
Yoshiaki S. Kato ◽  
Kazuhiko Kume
Keyword(s):  
Drosophila Melanogaster ◽  
Synaptic Contact ◽  
Brain Regions ◽  
Central Complex ◽  
Neuronal Circuit ◽  
Sleep Regulation ◽  
Protocerebral Bridge ◽  
Dopamine Signaling

The central complex is one of the major brain regions that control sleep in Drosophila. However, the circuitry details of sleep regulation have not been elucidated yet. Here, we show a novel sleep-regulating neuronal circuit in the protocerebral bridge (PB) of the central complex. Activation of the PB interneurons labeled by the R59E08-Gal4 and the PB columnar neurons with R52B10-Gal4 promoted sleep and wakefulness, respectively. A targeted GFP reconstitution across synaptic partners (t-GRASP) analysis demonstrated synaptic contact between these two groups of sleep-regulating PB neurons. Furthermore, we found that activation of a pair of dopaminergic (DA) neurons projecting to the PB (T1 DA neurons) decreased sleep. The wake-promoting T1 DA neurons and the sleep-promoting PB interneurons formed close associations. Dopamine 2-like receptor (Dop2R) knockdown in the sleep-promoting PB interneurons increased sleep. These results indicated that the neuronal circuit in the PB, regulated by dopamine signaling, mediates sleep-wakefulness.

scholarly journals Protocerebral bridge neurons that regulate sleep in Drosophila melanogaster

2020 ◽  
Author(s):  
Jun Tomita ◽  
Gosuke Ban ◽  
Yoshiaki S. Kato ◽  
Kazuhiko Kume
Keyword(s):  
Drosophila Melanogaster ◽  
Brain Regions ◽  
Central Complex ◽  
Neuronal Circuit ◽  
Sleep Regulation ◽  
Synaptic Contacts ◽  
Protocerebral Bridge ◽  
Dopamine Signaling

AbstractThe central complex is one of the major brain regions that control sleep in Drosophila, but the circuitry details of sleep regulation have yet to be elucidated. Here, we show a novel sleep-regulating neuronal circuit in the protocerebral bridge (PB) of the central complex. Activation of the PB interneurons labeled by the R59E08-Gal4 and the PB columnar neurons in the R52B10-Gal4 promoted sleep and wakefulness, respectively. A targeted GFP reconstitution across synaptic partners (t-GRASP) analysis demonstrated synaptic contacts between these two groups of sleep-regulating PB neurons. Furthermore, we found that activation of a pair of dopaminergic (DA) neurons projecting to the PB (T1 DA neurons) decreased sleep. The wake-promoting T1 DA neurons and the sleep-promoting PB interneurons formed close associations. Dopamine 2-like receptor (Dop2R) knockdown in the sleep-promoting PB interneurons increased sleep. These results indicated that the neuronal circuit in the PB regulated by dopamine signaling mediates sleep-wakefulness.

scholarly journals A neuronal circuit for vector computation builds an allocentric traveling-direction signal in the Drosophila fan-shaped body

2020 ◽  
Author(s):  
Cheng Lyu ◽  
L.F. Abbott ◽  
Gaby Maimon
Keyword(s):  
Computational Models ◽  
Neuronal Population ◽  
The Body ◽  
Central Complex ◽  
Two Dimensional ◽  
Neuronal Circuit ◽  
Head Direction ◽  
Neural Signals ◽  
Shaped Body ◽  
External Cues

AbstractMany behavioral tasks require the manipulation of mathematical vectors, but, outside of computational models1–8, it is not known how brains perform vector operations. Here we show how the Drosophila central complex, a region implicated in goal-directed navigation8–14, performs vector arithmetic. First, we describe neural signals in the fan-shaped body that explicitly track a fly’s allocentric traveling direction, that is, the traveling direction in reference to external cues. Past work has identified neurons in Drosophila12,15–17 and mammals18,19 that track allocentric heading (e.g., head-direction cells), but these new signals illuminate how the sense of space is properly updated when traveling and heading angles differ. We then characterize a neuronal circuit that rotates, scales, and adds four vectors related to the fly’s egocentric traveling direction–– the traveling angle referenced to the body axis––to compute the allocentric traveling direction. Each two-dimensional vector is explicitly represented by a sinusoidal activity pattern across a distinct neuronal population, with the sinusoid’s amplitude representing the vector’s length and its phase representing the vector’s angle. The principles of this circuit, which performs an egocentric-to-allocentric coordinate transformation, may generalize to other brains and to domains beyond navigation where vector operations or reference-frame transformations are required.

scholarly journals Differential modulation of NREM sleep regulation and EEG topography by chronic sleep restriction in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bowon Kim ◽  
Eunjin Hwang ◽  
Robert E. Strecker ◽  
Jee Hyun Choi ◽  
Youngsoo Kim
Keyword(s):  
Nrem Sleep ◽  
Brain Regions ◽  
Sleep Eeg ◽  
Sleep Restriction ◽  
Electrode Arrays ◽  
Sleep Regulation ◽  
Amplitude Analysis ◽  
Delta Power ◽  
Eeg Topography ◽  
Chronic Sleep

AbstractCompensatory elevation in NREM sleep EEG delta power has been typically observed following prolonged wakefulness and widely used as a sleep homeostasis indicator. However, recent evidence in human and rodent chronic sleep restriction (CSR) studies suggests that NREM delta power is not progressively increased despite of accumulated sleep loss over days. In addition, there has been little progress in understanding how sleep EEG in different brain regions responds to CSR. Using novel high-density EEG electrode arrays in the mouse model of CSR where mice underwent 18-h sleep deprivation per day for 5 consecutive days, we performed an extensive analysis of topographical NREM sleep EEG responses to the CSR condition, including period-amplitude analysis of individual slow waves. As previously reported in our analysis of REM sleep responses, we found different patterns of changes: (i) progressive decrease in NREM sleep duration and consolidation, (ii) persistent enhancement in NREM delta power especially in the frontal and parietal regions, and (iii) progressive increases in individual slow wave slope and frontal fast oscillation power. These results suggest that multiple sleep-wake regulatory systems exist in a brain region-specific manner, which can be modulated independently, especially in the CSR condition.

scholarly journals Differential modulation of global and local neural oscillations in REM sleep by homeostatic sleep regulation

2017 ◽  
Vol 114 (9) ◽  
pp. E1727-E1736 ◽  
Author(s):  
Bowon Kim ◽  
Bernat Kocsis ◽  
Eunjin Hwang ◽  
Youngsoo Kim ◽  
Robert E. Strecker ◽  
...  
Keyword(s):  
Rem Sleep ◽  
Brain Regions ◽  
Behavioral Pattern ◽  
Sleep Regulation ◽  
Slow Oscillations ◽  
Synaptic Homeostasis ◽  
Cortical Regions ◽  
Function Of Sleep ◽  
Fast Oscillations ◽  
Global And Local

Homeostatic rebound in rapid eye movement (REM) sleep normally occurs after acute sleep deprivation, but REM sleep rebound settles on a persistently elevated level despite continued accumulation of REM sleep debt during chronic sleep restriction (CSR). Using high-density EEG in mice, we studied how this pattern of global regulation is implemented in cortical regions with different functions and network architectures. We found that across all areas, slow oscillations repeated the behavioral pattern of persistent enhancement during CSR, whereas high-frequency oscillations showed progressive increases. This pattern followed a common rule despite marked topographic differences. The findings suggest that REM sleep slow oscillations may translate top-down homeostatic control to widely separated brain regions whereas fast oscillations synchronizing local neuronal ensembles escape this global command. These patterns of EEG oscillation changes are interpreted to reconcile two prevailing theories of the function of sleep, synaptic homeostasis and sleep dependent memory consolidation.

scholarly journals Impact of insulin signaling and proteasomal activity on physiological output of a neuronal circuit in aging Drosophila melanogaster

2018 ◽  
Vol 66 ◽  
pp. 149-157 ◽  
Author(s):  
Hrvoje Augustin ◽  
Kieran McGourty ◽  
Marcus J. Allen ◽  
Jennifer Adcott ◽  
Chi Tung Wong ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Insulin Signaling ◽  
Neuronal Circuit ◽  
Proteasomal Activity

No-Bridge of Drosophila Melanogaster: Portrait of a Structural Brain Mutant of the Central Complex

1992 ◽  
Vol 8 (3) ◽  
pp. 125-155 ◽  
Author(s):  
Roland Strauss ◽  
Ulrike Hanesch ◽  
Martin Kinkelin ◽  
Reinhard Wolf ◽  
Martin Heisenberg
Keyword(s):  
Drosophila Melanogaster ◽  
Central Complex ◽  
Structural Brain

scholarly journals Neuropeptide F regulates courtship in Drosophila through a male-specific neuronal circuit

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Weiwei Liu ◽  
Anindya Ganguly ◽  
Jia Huang ◽  
Yijin Wang ◽  
Jinfei D Ni ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Synaptic Connections ◽  
Neuronal Circuit ◽  
Male Courtship ◽  
Mating Experience ◽  
Sexual Drive ◽  
Decision Center ◽  
Receptor Neurons ◽  
Neuropeptide F ◽  
Male Specific

Male courtship is provoked by perception of a potential mate. In addition, the likelihood and intensity of courtship are influenced by recent mating experience, which affects sexual drive. Using Drosophila melanogaster, we found that the homolog of mammalian neuropeptide Y, neuropeptide F (NPF), and a cluster of male-specific NPF (NPFM) neurons, regulate courtship through affecting courtship drive. Disrupting NPF signaling produces sexually hyperactive males, which are resistant to sexual satiation, and whose courtship is triggered by sub-optimal stimuli. We found that NPFM neurons make synaptic connections with P1 neurons, which comprise the courtship decision center. Activation of P1 neurons elevates NPFM neuronal activity, which then act through NPF receptor neurons to suppress male courtship, and maintain the proper level of male courtship drive.

scholarly journals Epigenetic mediation of AKT1 rs1130233 s effect on delta-9-tetrahydrocannabinol-induced medial temporal function during fear processing

2021 ◽  
Author(s):  
Grace Blest-Hopley ◽  
Marco Colizzi ◽  
Diana Prata ◽  
Vincent Giampietro ◽  
Michael Brammer ◽  
...  
Keyword(s):  
Brain Function ◽  
Brain Regions ◽  
Parahippocampal Gyrus ◽  
Double Blind ◽  
Single Nucleotide ◽  
Epigenetic Methylation ◽  
Temporal Function ◽  
Dopamine Signaling ◽  
High Doses ◽  
Epigenetic Modulation

High doses of delta-9-tetrahydrocannabinol (THC), the main psychoactive component of cannabis, have been shown to have anxiogenic effects. Also, THC effects have been shown to be modulated by genotype, including the single nucleotide polymorphism (SNP) rs1130233 at the protein kinase AKT1 gene, a key component of the dopamine signaling cascade. As such, it is likely that epigenetic methylation around this SNP may affect AKT gene expression, which may in turn impact on the acute effects of THC on brain function. We investigated the genetic (AKT1 rs1130233) and epigenetic modulation of brain function during fear processing in a 2-session, double-blind, cross-over, randomized placebo-controlled THC administration, in 36 healthy males. Fear processing was assessed using an emotion (fear processing) paradigm, under functional magnetic resonance imaging (fMRI). Complete genetic and fMRI data was available for 34 participants. THC caused an increase in anxiety and transient psychotomimetic symptoms and para-hippocampal gyrus/ amygdala activation. Number of A alleles at the AKT1 rs1130233 SNP, and percentage methylation at the CpG11-12 site, were independently associated with a greater effect of THC on activation in a network of brain regions including left and right parahippocampal gyri, respectively. AKT1 rs1130233 moderation of the THC effect on left parahippocampal activation persisted after covarying for methylation percentage, and was partially mediated in sections of the left parahippocampal gyrus/ hippocampus by methylation percentage. These results may offer an example of how genetic and epigenetic variations influence the psychotomimetic and neurofunctional effects of THC.

Sign in / Sign up

Export Citation Format

Share Document