Sleep is differently modulated by basal forebrain GABAA and GABAB receptors

2001 ◽  
Vol 281 (1) ◽  
pp. R170-R175 ◽  
Author(s):  
Alfredo Manfridi ◽  
Dario Brambilla ◽  
Mauro Mancia
Keyword(s):  
Basal Forebrain ◽  
Slow Wave Sleep ◽  
Gabab Receptors ◽  
Nucleus Basalis ◽  
Receptor Subtype ◽  
Sleep Regulation ◽  
Sleep Parameters ◽  
Polygraphic Recordings ◽  
Sleep Modulation

There is evidence that GABA plays a major role in sleep regulation. GABAA receptor agonists and different compounds interacting with the GABAA receptor complex, such as barbiturates and benzodiazepines, can interfere with the sleep/wake cycle. On the other hand, there is very little information about the possible role of GABAB receptors in sleep modulation. The nucleus basalis of Meynert (NBM), a cholinergic area in the basal forebrain, plays a pivotal role in the modulation of sleep and wakefulness, and both GABAA and GABABreceptors have been described within the NBM. This study used unilateral infusions in the NBM to determine the effects of 3-hydroxy-5-aminomethylisoxazole hydrobromide (muscimol hydrobromide, a GABAA receptor subtype agonist) and β-(aminomethyl)-4-chlorobenzenepropanoic acid (baclofen, a GABAB receptor subtype agonist) on sleep parameters in freely moving rats by means of polygraphic recordings. Muscimol (0.5 nmol) and baclofen (0.7 nmol) induced an increase in slow-wave sleep and an inhibition of wakefulness. Muscimol, but not baclofen, also caused a decrease in desynchronized sleep parameters. The results reported here indicate that 1) the NBM activation of both GABAA and GABAB receptors influences the sleep/wake cycle, and 2) GABAA but not GABAB receptors are important for desynchronized sleep modulation, suggesting that the two GABAergic receptors play different roles in sleep modulation.

mRNA expression in mouse hypothalamus and basal forebrain during influenza infection: a novel model for sleep regulation

2006 ◽  
Vol 24 (3) ◽  
pp. 225-234 ◽  
Author(s):  
Ming Ding ◽  
Linda A. Toth
Keyword(s):  
Basal Forebrain ◽  
Slow Wave Sleep ◽  
Inbred Mice ◽  
Influenza Infection ◽  
Dark Phase ◽  
Potential Candidate ◽  
Lipocalin 2 ◽  
Sleep Regulation ◽  
Light Phase ◽  
Potential Candidate Gene

After influenza infection, C57BL/6J mice develop increased slow-wave sleep (SWS) during the dark phase of the day-night cycle, whereas BALB/cByJ mice develop decreased SWS during the light phase. A previous analysis of CXB recombinant inbred mice revealed a quantitative trait locus (QTL) designated Srilp (sleep response to influenza, light phase) that was related to expression of the BALB/cByJ sleep phenotype. Srilp was localized to the 10- to 12-cM region of mouse Chr 6 between D6Mit74 and D6Mit188. Temt (thioether S-methyltransferase), which is located at region B3 of Chr 6, is a potential candidate gene for Srilp. We evaluated the expression of Temt and other Srilp candidate genes in hypothalamus and basal forebrain of uninfected and influenza-infected C57BL/6J and BALB/cByJ mice. We report here that Temt expression varies significantly with respect to mouse strain, health status, brain region, and day-night phase. C57BL/6J mice show day-night variation in Temt expression in hypothalamus, but BALB/cByJ mice do not. Temt expression in basal forebrain is much higher in C57BL/6J mice than in BALB/cByJ mice. During influenza infection, both C57BL/6J and BALB/cByJ mice show reduced Temt mRNA in basal forebrain at 30 h postinoculation, but expression remains much lower in the BALB/cByJ strain. In contrast, prostaglandin-d-synthase ( Ptgds) and lipocalin 2 ( Lcn2) mRNA increase in basal forebrain of both strains after influenza infection. Administration of the TEMT inhibitor sinefungin reduces sleep in uninfected BALB/cByJ mice and attenuates influenza-induced sleep enhancement in C57BL/6J mice. These data suggest that strain- and infection-related alterations in sleep may be influenced by Temt expression and perhaps by subsequent effects on prostaglandin metabolism.

Stimulation of NMDA and AMPA receptors in the rat nucleus basalis of Meynert affects sleep

1999 ◽  
Vol 277 (5) ◽  
pp. R1488-R1492 ◽  
Author(s):  
Alfredo Manfridi ◽  
Dario Brambilla ◽  
Mauro Mancia
Keyword(s):  
Nmda Receptors ◽  
Glutamate Receptors ◽  
Ampa Receptors ◽  
Slow Wave Sleep ◽  
Nmda Antagonist ◽  
Nucleus Basalis ◽  
Nucleus Basalis Of Meynert ◽  
Mediated Effects ◽  
Polygraphic Recordings ◽  
Freely Moving

The nucleus basalis of Meynert (NBM), a heterogeneous area in the basal forebrain involved in the modulation of sleep and wakefulness, is rich in glutamate receptors, and glutamatergic fibers represent an important part of the input to this nucleus. With the use of unilateral infusions in the NBM, the effects of two different glutamatergic subtype agonists, namely N-methyl-d-aspartic acid (NMDA) and α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) hydrobromide, on sleep and wakefulness parameters were determined in freely moving rats by means of polygraphic recordings. NMDA (5 nmol) and AMPA (0.4 nmol) induced an increase in wakefulness and an inhibition of slow-wave sleep. AMPA, but not NMDA, also caused a decrease in desynchronized sleep. These AMPA- and NMDA-mediated effects were counteracted by a pretreatment with the specific NMDA antagonist 2-amino-5-phosphonopentanoic acid (20 nmol) and the specific AMPA antagonist 6,7-dinitroquinoxaline-2,3-dione (2 nmol), respectively. The results reported here indicate that 1) the NBM activation of both NMDA and AMPA glutamate receptors exert a modulatory influence on sleep and wakefulness, and 2) AMPA, but not NMDA receptors, are involved in the modulation of desynchronized sleep, suggesting a different role for NBM NMDA and non-NMDA receptors in sleep modulation.

Polysomnographic Findings in Nights Preceding a Migraine Attack

Cephalalgia ◽  
2001 ◽  
Vol 21 (1) ◽  
pp. 31-37 ◽  
Author(s):  
R Göder ◽  
G Fritzer ◽  
A Kapsokalyvas ◽  
P Kropp ◽  
U Niederberger ◽  
...  
Keyword(s):  
Slow Wave Sleep ◽  
Power Spectra ◽  
Cortical Activation ◽  
Alpha Power ◽  
Sleep Regulation ◽  
Beta Power ◽  
Rem Density ◽  
Sleep Parameters ◽  
Sleep Alterations ◽  
Electroencephalogram Eeg

Sleep recordings were performed in eight patients to analyse sleep alterations preceding migraine attacks. Polysomnographic recordings from nights before an attack were compared with nights without following migraine. We analysed standard sleep parameters and electroencephalogram (EEG) power spectra. The main findings preceding migraine attacks were a significant decrease in the number of arousals, a decrease in rapid eye movement (REM) density, a significant decrease of beta power in the slow wave sleep, and a decrease of alpha power during the first REM period. The results suggest a decrease in cortical activation during sleep preceding migraine attacks. According to the models of sleep regulation, alterations in the function of aminergic or cholinergic brainstem nuclei have to be discussed.

Role of the Basal Forebrain Cholinergic Projection in Somatosensory Cortical Plasticity

1998 ◽  
Vol 79 (6) ◽  
pp. 3216-3228 ◽  
Author(s):  
Robert N. S. Sachdev ◽  
Shao-Ming Lu ◽  
Ron G. Wiley ◽  
Ford F. Ebner
Keyword(s):  
Synaptic Plasticity ◽  
Basal Forebrain ◽  
Cortical Plasticity ◽  
Cortical Cell ◽  
Growth Factor Receptor ◽  
Nucleus Basalis ◽  
Adult Rats ◽  
Cholinergic Basal Forebrain ◽  
Cholinergic Projection

Sachdev, Robert N. S., Shao-Ming Lu, Ron G. Wiley, and Ford F. Ebner. Role of the basal forebrain cholinergic projection in somatosensory cortical plasticity. J. Neurophysiol. 79: 3216–3228, 1998. Trimming all but two whiskers in adult rats produces a predictable change in cortical cell-evoked responses characterized by increased responsiveness to the two intact whiskers and decreased responsiveness to the trimmed whiskers. This type of synaptic plasticity in rat somatic sensory cortex, called “whisker pairing plasticity,” first appears in cells above and below the layer IV barrels. These are also the cortical layers that receive the densest cholinergic inputs from the nucleus basalis. The present study assesses whether the cholinergic inputs to cortex have a role in regulating whisker pairing plasticity. To do this, cholinergic basal forebrain fibers were eliminated using an immunotoxin specific for these fibers. A monoclonal antibody to the low-affinity nerve growth factor receptor 192 IgG, conjugated to the cytotoxin saporin, was injected into cortex to eliminate cholinergic fibers in the barrel field. The immunotoxin reduces acetylcholine esterase (AChE)-positive fibers in S1 cortex by >90% by 3 wk after injection. Sham-depleted animals in which either saporin alone or saporin unconjugated to 192 IgG is injected into the cortex produces no decrease in AChE-positive fibers in cortex. Sham-depleted animals show the expected plasticity in barrel column neurons. In contrast, no plasticity develops in the ACh-depleted, 7-day whisker-paired animals. These results support the conclusion that the basal forebrain cholinergic projection to cortex is an important facilitator of synaptic plasticity in mature cortex.

Spontaneous, homeostatic, and inflammation-induced sleep in NF-κB p50 knockout mice

2006 ◽  
Vol 291 (5) ◽  
pp. R1516-R1526 ◽  
Author(s):  
K. A. Jhaveri ◽  
V. Ramkumar ◽  
R. A. Trammell ◽  
L. A. Toth
Keyword(s):  
Transcription Factor ◽  
Influenza Virus ◽  
Slow Wave Sleep ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Immune Challenge ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Transcription Factor Nuclear Factor

The dimeric transcription factor nuclear factor-κB (NF-κB) regulates several endogenous sleep-modulatory substances and thereby serves as a pivotal mediator of sleep-wake homeostasis. To further define the role of NF-κB in sleep regulation, we monitored sleep and temperature in mice that lack the p50 subunit of NF-κB [p50 knockout (KO) mice]. Compared with the control B6129PF2/J strain, p50 KO mice spend more time in slow-wave sleep (SWS) and rapid eye movement sleep (REMS) under normal conditions and show enhanced homeostatic recovery of sleep after sleep loss. p50 KO mice also show increased SWS and reduced REMS and temperature after the administration of lipopolysaccharide, yet they are behaviorally less responsive to challenge with influenza virus. These data support a role for NF-κB, and, in particular, for the p50 subunit, in the regulation of sleep in healthy mice and in mice experiencing immune challenge.

scholarly journals Blood and brain magnesium in inbred mice and their correlation with sleep quality

2000 ◽  
Vol 279 (6) ◽  
pp. R2173-R2178 ◽  
Author(s):  
Didier Chollet ◽  
Paul Franken ◽  
Yvette Raffin ◽  
Alain Malafosse ◽  
Jean Widmer ◽  
...  
Keyword(s):  
Sleep Quality ◽  
Slow Wave Sleep ◽  
Inbred Mice ◽  
Recovery Process ◽  
Brain Structures ◽  
Inbred Strains ◽  
Sleep Regulation ◽  
Specific Distribution ◽  
Before And After ◽  
Sleep Parameters

A strong genetic component in the regulation of blood magnesium (Mg) levels has been demonstrated. The regulation and distribution of brain Mg levels, however, have never been assessed. Herein we report on the genetic variation of peripheral and central Mg levels in six inbred strains of mice. In addition, the possible involvement of Mg in sleep regulation was assessed by establishing correlations between Mg and sleep parameters obtained before and after a 6-h sleep deprivation. Although genotype strongly determined blood Mg levels, it did not affect brain Mg, suggesting that central and peripheral Mg are regulated differently. Central Mg displayed a highly structure-specific distribution with frontal cortex having the highest and brain stem the lowest values. Whereas for the amount and distribution of baseline sleep only marginal correlations with Mg were found, Mg contents in four of nine brain structures were highly positively correlated with the length of slow-wave sleep episodes during recovery. This relationship suggests that higher levels of Mg in specific brain sites promote sleep quality as part of a recovery process.

Assessment for the Role of Serotonin Receptor Subtype 3 for the Analgesic Action of Morphine at the Spinal Level

2005 ◽  
Vol 18 (2) ◽  
pp. 113
Author(s):  
Myung Ha Yoon ◽  
Hong Buem Bae ◽  
Jeong Il Choi ◽  
Seok Jae Kim ◽  
Chang Mo Kim ◽  
...  
Keyword(s):  
Serotonin Receptor ◽  
Receptor Subtype ◽  
Analgesic Action ◽  
Spinal Level ◽  
Subtype 3

Vitamin D and Sleep Regulation: Is there a Role for Vitamin D?

2020 ◽  
Vol 26 (21) ◽  
pp. 2492-2496 ◽  
Author(s):  
Fiammetta Romano ◽  
Giovanna Muscogiuri ◽  
Elea Di Benedetto ◽  
Volha V. Zhukouskaya ◽  
Luigi Barrea ◽  
...  
Keyword(s):  
Vitamin D ◽  
Sleep Disorders ◽  
Vitamin D Deficiency ◽  
Sleep Apnea Syndrome ◽  
Regulatory Mechanisms ◽  
Sleep Regulation ◽  
Vitamin D Receptors ◽  
Obstructive Sleep ◽  
The Impact

Background: Vitamin D exerts multiple pleiotropic effects beyond its role in calcium-phosphate metabolism. Growing evidence suggests an association between hypovitaminosis D and sleep disorders, thus increasing the interest in the role of this vitamin in the regulatory mechanisms of the sleep-wake cycle. Objective: The study aimed to explore and summarize the current knowledge about the role of vitamin D in sleep regulation and the impact of vitamin D deficiency on sleep disorders. Methods: The main regulatory mechanisms of vitamin D on sleep are explained in this study. The literature was scanned to identify clinical trials and correlation studies showing an association between vitamin D deficiency and sleep disorders. Results: Vitamin D receptors and the enzymes that control their activation and degradation are expressed in several areas of the brain involved in sleep regulation. Vitamin D is also involved in the pathways of production of Melatonin, the hormone involved in the regulation of human circadian rhythms and sleep. Furthermore, vitamin D can affect sleep indirectly through non-specific pain disorders, correlated with alterations in sleep quality, such as restless legs syndrome and obstructive sleep apnea syndrome. Conclusions: : Vitamin D has both a direct and an indirect role in the regulation of sleep. Although vitamin D deficiency has been associated to sleep disorders, there is still scant evidence to concretely support the role of vitamin D supplementation in the prevention or treatment of sleep disturbances; indeed, more intervention studies are needed to better clarify these aspects.

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