Gene expression analysis in the mouse brainstem identifies Cart and Nesfatin as neuropeptides coexpressed in the Calbindin-positive neurons of the Nucleus papilio

Abstract Study Objectives: The brainstem contains several neuronal populations, heterogeneous in terms of neurotransmitter/neuropeptide content, which are important for controlling various aspects of the rapid eye movement (REM) phase of sleep. Among these populations are the Calbindin (Calb)-immunoreactive NPCalb neurons, located in the Nucleus papilio, within the dorsal paragigantocellular nucleus (DPGi), and recently shown to control eye movement during the REM phase of sleep. Methods: We performed in-depth data mining of the in situ hybridization data collected at the Allen Brain Atlas, in order to identify potentially interesting genes expressed in this brainstem nucleus. Our attention focused on genes encoding neuropeptides, including Cart (Cocaine and Amphetamine Regulated Transcripts) and Nesfatin 1. Results: While nesfatin 1 appeared ubiquitously expressed in this Calb-positive neuronal population, Cart was coexpressed in only a subset of these glutamatergic NPCalb neurons. Furthermore, an REM sleep deprivation and rebound assay performed with mice revealed that the Cart-positive neuronal population within the DPGi was activated during REM sleep (as measured by c-fos immunoreactivity), suggesting a role of this neuropeptide in regulating some aspects of REM sleep. Conclusions: The assembled information could afford functional clues to investigators, conducive to further experimental pursuits.

Download Full-text

Rapid eye movement (REM) sleep deprivation reduces rat frontal cortex acetylcholinesterase (EC 3.1.1.7) activity

Brazilian Journal of Medical and Biological Research ◽

10.1590/s0100-879x1997000500012 ◽

1997 ◽

Vol 30 (5) ◽

pp. 641-647 ◽

Cited By ~ 5

Author(s):

R. Camarini ◽

M.A.C. Benedito

Keyword(s):

Sleep Deprivation ◽

Frontal Cortex ◽

Eye Movement ◽

Rem Sleep ◽

Rapid Eye Movement ◽

Rem Sleep Deprivation ◽

Rat Frontal Cortex

Download Full-text

Noradrenergic activity in rat brain during rapid eye movement sleep deprivation and rebound sleep

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1995.268.6.r1456 ◽

1995 ◽

Vol 268 (6) ◽

pp. R1456-R1463 ◽

Cited By ~ 11

Author(s):

T. Porkka-Heiskanen ◽

S. E. Smith ◽

T. Taira ◽

J. H. Urban ◽

J. E. Levine ◽

...

Keyword(s):

Sleep Deprivation ◽

Eye Movement ◽

Rem Sleep ◽

High Performance ◽

Locus Ceruleus ◽

Rapid Eye Movement ◽

Rem Sleep Deprivation ◽

Large Platform ◽

Male Wistar Rats ◽

Th Mrna

Noradrenergic locus ceruleus neurons are most active during waking and least active during rapid eye movement (REM) sleep. We expected REM sleep deprivation (REMSD) to increase norepinephrine utilization and activate the tyrosine hydroxylase (TH) gene critical for norepinephrine production. Male Wistar rats were deprived of REM sleep with the platform method. Rats were decapitated after 8, 24, or 72 h on small (REMSD) or large (control) platforms or after 8 or 24 h of rebound sleep after 72 h of the platform treatment. During the first 24 h, norepinephrine concentration, measured by high-performance liquid chromatography/electrochemical detection, was lower in the neocortex, hippocampus, and posterior hypothalamus in REMSD rats than in large-platform controls. After 72 h of REMSD, TH mRNA, measured by in situ hybridization, was increased in the locus ceruleus and norepinephrine concentrations were increased. Polygraphy showed that small-platform treatment caused effective and selective REMSD. Serum corticosterone measurement by radioimmunoassay indicated that the differences found in norepinephrine and TH mRNA were not due to differences in stress between the treatments. The novel finding of sleep deprivation-specific increase in TH gene expression indicates an important mechanism of adjusting to sleep deprivation.

Download Full-text

Pathway-dependent regulation of sleep dynamics in a network model of the sleep-wake cycle

10.1101/705822 ◽

2019 ◽

Cited By ~ 1

Author(s):

Charlotte Héricé ◽

Shuzo Sakata

Keyword(s):

Computational Model ◽

Eye Movement ◽

Network Model ◽

Rem Sleep ◽

Synaptic Weight ◽

Nrem Sleep ◽

Cell Types ◽

Brain Areas ◽

Neuronal Populations ◽

Neural Populations

AbstractSleep is a fundamental homeostatic process within the animal kingdom. Although various brain areas and cell types are involved in the regulation of the sleep-wake cycle, it is still unclear how different pathways between neural populations contribute to its regulation. Here we address this issue by investigating the behavior of a simplified network model upon synaptic weight manipulations. Our model consists of three neural populations connected by excitatory and inhibitory synapses. Activity in each population is described by a firing-rate model, which determines the state of the network. Namely wakefulness, rapid eye movement (REM) sleep or non-REM (NREM) sleep. By systematically manipulating the synaptic weight of every pathway, we show that even this simplified model exhibits non-trivial behaviors: for example, the wake-promoting population contributes not just to the induction and maintenance of wakefulness, but also to sleep induction. Although a recurrent excitatory connection of the REM-promoting population is essential for REM sleep genesis, this recurrent connection does not necessarily contribute to the maintenance of REM sleep. The duration of NREM sleep can be shortened or extended by changes in the synaptic strength of the pathways from the NREM-promoting population. In some cases, there is an optimal range of synaptic strengths that affect a particular state, implying that the amount of manipulations, not just direction (i.e., activation or inactivation), needs to be taken into account. These results demonstrate pathway-dependent regulation of sleep dynamics and highlight the importance of systems-level quantitative approaches for sleep-wake regulatory circuits.Author SummarySleep is essential and ubiquitous across animal species. Over the past half-century, various brain areas, cell types, neurotransmitters, and neuropeptides have been identified as part of a sleep-wake regulating circuitry in the brain. However, it is less explored how individual neural pathways contribute to the sleep-wake cycle. In the present study, we investigate the behavior of a computational model by altering the strength of connections between neuronal populations. This computational model is comprised of a simple network where three neuronal populations are connected together, and the activity of each population determines the current state of the model, that is, wakefulness, rapid-eye-movement (REM) sleep or non-REM (NREM) sleep. When we alter the connection strength of each pathway, we observe that the effect of such alterations on the sleep-wake cycle is highly pathway-dependent. Our results provide further insights into the mechanisms of sleep-wake regulation, and our computational approach can complement future biological experiments.

Download Full-text

The Role of GABAergic Modulation of Mesopontine Cholinergic Neurotransmission in Rapid Eye Movement (REM) Sleep

GABA and Sleep ◽

10.1007/978-3-0346-0226-6_12 ◽

2010 ◽

pp. 253-277

Author(s):

Gerald A Marks ◽

Christopher M Sinton

Keyword(s):

Eye Movement ◽

Rem Sleep ◽

Rapid Eye Movement ◽

Cholinergic Neurotransmission ◽

Gabaergic Modulation

Download Full-text

Role of Corticosterone on Sleep Homeostasis Induced by REM Sleep Deprivation in Rats

PLoS ONE ◽

10.1371/journal.pone.0063520 ◽

2013 ◽

Vol 8 (5) ◽

pp. e63520 ◽

Cited By ~ 15

Author(s):

Ricardo Borges Machado ◽

Sergio Tufik ◽

Deborah Suchecki

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Rem Sleep Deprivation ◽

Sleep Homeostasis

Download Full-text

Prophylactic Role of Oral Melatonin Administration on Neurogenesis in Adult Balb/C Mice during REM Sleep Deprivation

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/2136902 ◽

2016 ◽

Vol 2016 ◽

pp. 1-10 ◽

Cited By ~ 6

Author(s):

Gabriela López-Armas ◽

Mario Eduardo Flores-Soto ◽

Verónica Chaparro-Huerta ◽

Luis Felipe Jave-Suarez ◽

Sofía Soto-Rodríguez ◽

...

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Neural Progenitors ◽

Control Group ◽

Rem Sleep Deprivation ◽

Melatonin Concentration ◽

Antiapoptotic Proteins ◽

Adult Mice ◽

Melatonin Administration

Purpose. The aim of this study was to assess the effect of melatonin in the proliferation of neural progenitors, melatonin concentration, and antiapoptotic proteins in the hippocampus of adult mice exposed to 96 h REM sleep deprivation (REMSD) prophylactic administration of melatonin for 14 days.Material and Methods. Five groups of Balb/C mice were used: (1) control, (2) REMSD, (3) melatonin (10 mg/kg) plus REMSD, (4) melatonin and intraperitoneal luzindole (once a day at 5 mg/kg) plus REMSD, and (5) luzindole plus REMSD. To measure melatonin content in hippocampal tissue we used HPLC. Bcl-2 and Bcl-xL proteins were measured by Western Blot and neurogenesis was determined by injecting 5-bromo-2-deoxyuridine (BrdU) and BrdU/nestin expressing cells in the subgranular zone of the dentate gyrus were quantified by epifluorescence.Results. The melatonin-treated REMSD group showed an increased neural precursor in 44% with respect to the REMSD group and in 28% when contrasted with the control group (P<0.021). The melatonin-treated REMSD group also showed the highest expression of Bcl-2 and Bcl-xL as compared to the rest of the groups.Conclusion. The exogenous administration of melatonin restores the tissue levels of sleep-deprived group and appears to be an efficient neuroprotective agent against the deleterious effects of REMSD.

Download Full-text

Critical role of CA1 muscarinic receptors on memory acquisition deficit induced by total (TSD) and REM sleep deprivation (RSD)

Progress in Neuro-Psychopharmacology and Biological Psychiatry ◽

10.1016/j.pnpbp.2017.05.024 ◽

2017 ◽

Vol 79 ◽

pp. 128-135 ◽

Cited By ~ 9

Author(s):

Bibi-Zahra Javad-Moosavi ◽

Gholamhassan Vaezi ◽

Mohammad Nasehi ◽

Seyed-Ali Haeri-Rouhani ◽

Mohammad-Reza Zarrindast

Keyword(s):

Sleep Deprivation ◽

Muscarinic Receptors ◽

Rem Sleep ◽

Critical Role ◽

Rem Sleep Deprivation ◽

Memory Acquisition

Download Full-text

MATHEMATICAL PHASE MODEL OF NEURAL POPULATIONS INTERACTION IN MODULATION OF REM/NREM SLEEP

Mathematical Modelling and Analysis ◽

10.3846/13926292.2016.1247302 ◽

2016 ◽

Vol 21 (6) ◽

pp. 794-810 ◽

Cited By ~ 1

Author(s):

Paolo Acquistapace ◽

Anna P. Candeloro ◽

Vladimir Georgiev ◽

Maria L. Manca

Keyword(s):

Experimental Data ◽

Eye Movement ◽

Rem Sleep ◽

Reaction Diffusion ◽

Nrem Sleep ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep ◽

Neuronal Populations ◽

Neural Populations ◽

Cyclic Oscillation

Aim of the present study is to compare the synchronization of the classical Kuramoto system and the reaction - diffusion space time Landau - Ginzburg model, in order to describe the alternation of REM (rapid eye movement) and NREM (non-rapid eye movement) sleep across the night. These types of sleep are considered as produced by the cyclic oscillation of two neuronal populations that, alternatively, promote and inhibit the REM sleep. Even if experimental data will be necessary, a possible interpretation of the results has been proposed.

Download Full-text

REM sleep promotes experience-dependent dendritic spine elimination in the mouse cortex

Nature Communications ◽

10.1038/s41467-020-18592-5 ◽

2020 ◽

Vol 11 (1) ◽

Cited By ~ 2

Author(s):

Yanmei Zhou ◽

Cora Sau Wan Lai ◽

Yang Bai ◽

Wei Li ◽

Ruohe Zhao ◽

...

Keyword(s):

Sleep Deprivation ◽

Neuronal Activity ◽

Rem Sleep ◽

Dendritic Spine ◽

Monocular Deprivation ◽

Association Cortex ◽

Synapse Elimination ◽

Rem Sleep Deprivation ◽

Calcium Spikes

Abstract In many parts of the nervous system, experience-dependent refinement of neuronal circuits predominantly involves synapse elimination. The role of sleep in this process remains unknown. We investigated the role of sleep in experience-dependent dendritic spine elimination of layer 5 pyramidal neurons in the visual (V1) and frontal association cortex (FrA) of 1-month-old mice. We found that monocular deprivation (MD) or auditory-cued fear conditioning (FC) caused rapid spine elimination in V1 or FrA, respectively. MD- or FC-induced spine elimination was significantly reduced after total sleep or REM sleep deprivation. Total sleep or REM sleep deprivation also prevented MD- and FC-induced reduction of neuronal activity in response to visual or conditioned auditory stimuli. Furthermore, dendritic calcium spikes increased substantially during REM sleep, and the blockade of these calcium spikes prevented MD- and FC-induced spine elimination. These findings reveal an important role of REM sleep in experience-dependent synapse elimination and neuronal activity reduction.

Download Full-text