scholarly journals Differential regulation of the Drosophila sleep homeostat by circadian and arousal inputs

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Jinfei D Ni ◽  
Adishthi S Gurav ◽  
Weiwei Liu ◽  
Tyler H Ogunmowo ◽  
Hannah Hackbart ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Differential Regulation ◽  
Central Complex ◽  
Synaptic Connections ◽  
Circadian Pacemaker ◽  
Pacemaker Neurons ◽  
Synaptic Inputs ◽  
Shaped Body ◽  
Sleep Homeostat ◽  
The Brain

One output arm of the sleep homeostat in Drosophila appears to be a group of neurons with projections to the dorsal fan-shaped body (dFB neurons) of the central complex in the brain. However, neurons that regulate the sleep homeostat remain poorly understood. Using neurogenetic approaches combined with Ca2+ imaging, we characterized synaptic connections between dFB neurons and distinct sets of upstream sleep-regulatory neurons. One group of the sleep-promoting upstream neurons is a set of circadian pacemaker neurons that activates dFB neurons via direct glutaminergic excitatory synaptic connections. Opposing this population, a group of arousal-promoting neurons downregulates dFB axonal output with dopamine. Co-activating these two inputs leads to frequent shifts between sleep and wake states. We also show that dFB neurons release the neurotransmitter GABA and inhibit octopaminergic arousal neurons. We propose that dFB neurons integrate synaptic inputs from distinct sets of upstream sleep-promoting circadian clock neurons, and arousal neurons.

scholarly journals Coordinated activity of sleep and arousal neurons for stabilizing sleep/wake states in Drosophila

2018 ◽  
Author(s):  
Jinfei D. Ni ◽  
Tyler H. Ogunmowo ◽  
Hannah Hackbart ◽  
Ahmed Elsheikh ◽  
Adishthi S. Gurav ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Ex Vivo ◽  
Central Complex ◽  
List Type ◽  
Shaped Body ◽  
Sleep Homeostat ◽  
The Brain ◽  
Rapid Sleep

SummaryThe output arm of the sleep homeostat in Drosophila is a group of neurons with projections to the dorsal fan-shaped body (dFSB) of the central complex in the brain. However, neurons that regulate the sleep homeostat remain poorly understood. Using neurogenetic approaches combined with ex vivo Ca2+ imaging, we identify two groups of sleep-regulatory neurons that modulate the activity of the sleep homeostat in an opposing fashion. The sleep-promoting neurons activate the sleep homeostat with glutamate, whereas the arousal-promoting neurons down-regulate the sleep homeostat’s output with dopamine. Co-activating these two inputs leads to frequent shifts between sleep and wake states. We also show that dFSB sleep homeostat neurons release the neurotransmitter GABA that inhibits octopaminergic arousal neurons. Taken together, we suggest coordinated neuronal activity of sleep- and arousal-promoting neurons is essential for stabilizing sleep/wake states.HighlightsGlutamate released by AstA neurons activates dFSBAstAR1 sleep-promoting neuronsDopamine down-regulates the activity of dFSBAstAR1 neuronsSimultaneous glutamate and dopamine input causes rapid sleep and awake swingsGABA released by dFSBAstAR1 neurons promotes sleep by inhibiting arousal neurons

Hugin+ neurons provide a link between sleep homeostat and circadian clock neurons

2021 ◽  
Vol 118 (47) ◽  
pp. e2111183118
Author(s):  
Jessica E. Schwarz ◽  
Anna N. King ◽  
Cynthia T. Hsu ◽  
Annika F. Barber ◽  
Amita Sehgal
Keyword(s):  
Locomotor Activity ◽  
Sleep Deprivation ◽  
Circadian Clock ◽  
Sleep Loss ◽  
Daily Cycle ◽  
Shaped Body ◽  
Recovery Sleep ◽  
Sleep Homeostat ◽  
Central Clock ◽  
Homeostatic Mechanisms

Sleep is controlled by homeostatic mechanisms, which drive sleep after wakefulness, and a circadian clock, which confers the 24-h rhythm of sleep. These processes interact with each other to control the timing of sleep in a daily cycle as well as following sleep deprivation. However, the mechanisms by which they interact are poorly understood. We show here that hugin+ neurons, previously identified as neurons that function downstream of the clock to regulate rhythms of locomotor activity, are also targets of the sleep homeostat. Sleep deprivation decreases activity of hugin+ neurons, likely to suppress circadian-driven activity during recovery sleep, and ablation of hugin+ neurons promotes sleep increases generated by activation of the homeostatic sleep locus, the dorsal fan-shaped body (dFB). Also, mutations in peptides produced by the hugin+ locus increase recovery sleep following deprivation. Transsynaptic mapping reveals that hugin+ neurons feed back onto central clock neurons, which also show decreased activity upon sleep loss, in a Hugin peptide–dependent fashion. We propose that hugin+ neurons integrate circadian and sleep signals to modulate circadian circuitry and regulate the timing of sleep.

scholarly journals Light Affects the Branching Pattern of Peptidergic Circadian Pacemaker Neurons in the Brain of the Cockroach Leucophaea maderae

2011 ◽  
Vol 26 (6) ◽  
pp. 507-517 ◽  
Author(s):  
Hongying Wei ◽  
Monika Stengl
Keyword(s):  
Fruit Flies ◽  
Branching Pattern ◽  
Circadian Pacemaker ◽  
Pacemaker Neurons ◽  
Optic Lobes ◽  
Pigment Dispersing Factor ◽  
Accessory Medulla ◽  
Leucophaea Maderae ◽  
The Brain

Pigment-dispersing factor–immunoreactive neurons anterior to the accessory medulla (aPDFMes) in the optic lobes of insects are circadian pacemaker neurons in cockroaches and fruit flies. The authors examined whether any of the aPDFMes of the cockroach Leucophaea maderae are sensitive to changes in period and photoperiod of light/dark (LD) cycles as a prerequisite to adapt to changes in external rhythms. Cockroaches were raised in LD cycles of 11:11, 13:13, 12:12, 6:18, or 18:6 h, and the brains of the adults were examined with immunocytochemistry employing antisera against PDF and orcokinin. Indeed, in 11:11 LD cycles, only the number of medium-sized aPDFMes specifically decreased, while it increased in 13:13. In addition, 18:6 LD cycles increased the number of large- and medium-sized aPDFMes, as well as the posterior pPDFMes, while 6:18 LD cycles only decreased the number of medium-sized aPDFMes. Furthermore, PDF-immunoreactive fibers in the anterior optic commissure and orcokinin-immunoreactive fibers in both the anterior and posterior optic commissures were affected by different lengths of light cycles. Thus, apparently different groups of the PDFMes, most of all the medium-sized aPDFMes, which colocalize orcokinin, respond to changes in period and photoperiod and could possibly allow for the adjustment to different photoperiods.

scholarly journals Differential regulation of circadian pacemaker output by separate clock genes in Drosophila

2000 ◽  
Vol 97 (7) ◽  
pp. 3608-3613 ◽  
Author(s):  
J. H. Park ◽  
C. Helfrich-Forster ◽  
G. Lee ◽  
L. Liu ◽  
M. Rosbash ◽  
...  
Keyword(s):  
Clock Genes ◽  
Differential Regulation ◽  
Circadian Pacemaker

scholarly journals Ion Channels as New Attractive Targets to Improve Re-Myelination Processes in the Brain

2021 ◽  
Vol 22 (14) ◽  
pp. 7277
Author(s):  
Federica Cherchi ◽  
Irene Bulli ◽  
Martina Venturini ◽  
Anna Maria Pugliese ◽  
Elisabetta Coppi
Keyword(s):  
Ion Channels ◽  
Demyelinating Disease ◽  
Oligodendrocyte Progenitor Cells ◽  
Target Groups ◽  
Synaptic Inputs ◽  
Drug Actions ◽  
The Central Nervous System ◽  
Therapeutic Mechanisms ◽  
Voltage Gated Channels ◽  
The Brain

Multiple sclerosis (MS) is the most demyelinating disease of the central nervous system (CNS) characterized by neuroinflammation. Oligodendrocyte progenitor cells (OPCs) are cycling cells in the developing and adult CNS that, under demyelinating conditions, migrate to the site of lesions and differentiate into mature oligodendrocytes to remyelinate damaged axons. However, this process fails during disease chronicization due to impaired OPC differentiation. Moreover, OPCs are crucial players in neuro-glial communication as they receive synaptic inputs from neurons and express ion channels and neurotransmitter/neuromodulator receptors that control their maturation. Ion channels are recognized as attractive therapeutic targets, and indeed ligand-gated and voltage-gated channels can both be found among the top five pharmaceutical target groups of FDA-approved agents. Their modulation ameliorates some of the symptoms of MS and improves the outcome of related animal models. However, the exact mechanism of action of ion-channel targeting compounds is often still unclear due to the wide expression of these channels on neurons, glia, and infiltrating immune cells. The present review summarizes recent findings in the field to get further insights into physio-pathophysiological processes and possible therapeutic mechanisms of drug actions.

Central and Peripheral Clock Control of Circadian Feeding Rhythms

2021 ◽  
pp. 074873042110458
Author(s):  
Carson V. Fulgham ◽  
Austin P. Dreyer ◽  
Anita Nasseri ◽  
Asia N. Miller ◽  
Jacob Love ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Circadian Clock ◽  
Feeding Behavior ◽  
Molecular Clock ◽  
Fat Body ◽  
Molecular Clocks ◽  
Central Brain ◽  
Feeding Rhythms ◽  
Free Running ◽  
The Brain

Many behaviors exhibit ~24-h oscillations under control of an endogenous circadian timing system that tracks time of day via a molecular circadian clock. In the fruit fly, Drosophila melanogaster, most circadian research has focused on the generation of locomotor activity rhythms, but a fundamental question is how the circadian clock orchestrates multiple distinct behavioral outputs. Here, we have investigated the cells and circuits mediating circadian control of feeding behavior. Using an array of genetic tools, we show that, as is the case for locomotor activity rhythms, the presence of feeding rhythms requires molecular clock function in the ventrolateral clock neurons of the central brain. We further demonstrate that the speed of molecular clock oscillations in these neurons dictates the free-running period length of feeding rhythms. In contrast to the effects observed with central clock cell manipulations, we show that genetic abrogation of the molecular clock in the fat body, a peripheral metabolic tissue, is without effect on feeding behavior. Interestingly, we find that molecular clocks in the brain and fat body of control flies gradually grow out of phase with one another under free-running conditions, likely due to a long endogenous period of the fat body clock. Under these conditions, the period of feeding rhythms tracks with molecular oscillations in central brain clock cells, consistent with a primary role of the brain clock in dictating the timing of feeding behavior. Finally, despite a lack of effect of fat body selective manipulations, we find that flies with simultaneous disruption of molecular clocks in multiple peripheral tissues (but with intact central clocks) exhibit decreased feeding rhythm strength and reduced overall food intake. We conclude that both central and peripheral clocks contribute to the regulation of feeding rhythms, with a particularly dominant, pacemaker role for specific populations of central brain clock cells.

The novel guanylyl cyclase MsGC-I is strongly expressed in higher-order neuropils in the brain of Manduca sexta

2001 ◽  
Vol 204 (2) ◽  
pp. 305-314 ◽  
Author(s):  
A. Nighorn ◽  
P.J. Simpson ◽  
D.B. Morton
Keyword(s):  
Nervous System ◽  
Manduca Sexta ◽  
Guanylyl Cyclase ◽  
Higher Order ◽  
Adult Brain ◽  
Central Complex ◽  
Amino Acid Residues ◽  
Order Processing ◽  
Guanylyl Cyclases ◽  
The Brain

Guanylyl cyclases are usually characterized as being either soluble (sGCs) or receptor (rGCs). We have recently cloned a novel guanylyl cyclase, MsGC-I, from the developing nervous system of the hawkmoth Manduca sexta that cannot be classified as either an sGC or an rGC. MsGC-I shows highest sequence identity with receptor guanylyl cyclases throughout its catalytic and dimerization domains, but does not contain the ligand-binding, transmembrane or kinase-like domains characteristic of receptor guanylyl cyclases. In addition, MsGC-I contains a C-terminal extension of 149 amino acid residues. In this paper, we report the expression of MsGC-I in the adult. Northern blots show that it is expressed preferentially in the nervous system, with high levels in the pharate adult brain and antennae. In the antennae, immunohistochemical analyses show that it is expressed in the cell bodies and dendrites, but not axons, of olfactory receptor neurons. In the brain, it is expressed in a variety of sensory neuropils including the antennal and optic lobes. It is also expressed in structures involved in higher-order processing including the mushroom bodies and central complex. This complicated expression pattern suggests that this novel guanylyl cyclase plays an important role in mediating cyclic GMP levels in the nervous system of Manduca sexta.

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