GABAergic Regulation of REM Sleep in Reticularis Pontis Oralis and  Caudalis in Rats

Sanford, Larry D.; Tang, Xiangdong; Xiao, Jihua; Ross, Richard; Morrison, Adrian R.

doi:10.1152/jn.00993.2002

Cited by 82 publications

(102 citation statements)

References 20 publications

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“…The greater effects of CRH and AST on wakefulness and sleep in BALB/cJ mice compared to C57BL/6J mice are consistent with findings that BALB/cJ mice are more reactive in behavioral tests of anxiety (Belzung and Griebel, 2001;Tang et al, 2002b) and also show greater alterations in sleep in response to a number of stressors (Wurbel et al, 1998;Sanford et al, 2003a;2003b;2003d). Thus, strain differences in the effects of CRH and AST may be linked to underlying differences in the CRH system that may also be involved in the relative responsiveness to stressors in C57BL/6J and BALB/cJ mice.…”

Section: Discussionsupporting

confidence: 85%

“…In addition, exposure to an open field induced greater initial reductions with less subsequent increases in REM in BALB/cJ mice whereas C57BL/6J mice exhibited relatively less initial reductions but greater subsequent increases (Tang et al, 2004;. Based on these results, we suggested that the putative trait anxiety in BALB/ cJ mice might play a critical role in the relatively greater effects on REM induced by stressors (Liu et al, 2003;Sanford et al, 2003a;2003b;2003d;Liu et al, 2004;.…”

Section: Introductionmentioning

confidence: 61%

“…The relative magnitude and duration of the changes in sleep has been found to vary with strain. For example, compared to C57BL/6J mice, BALB/cJ mice display greater initial post-exposure reductions in REM following a variety of stressors (Wurbel et al, 1998;Sanford et al, 2003a;2003b;2003d). In addition, exposure to an open field induced greater initial reductions with less subsequent increases in REM in BALB/cJ mice whereas C57BL/6J mice exhibited relatively less initial reductions but greater subsequent increases (Tang et al, 2004;.…”

Section: Introductionmentioning

confidence: 98%

“…Indeed, BALB/cJ mice have been suggested to exhibit pathological anxiety (Belzung and Griebel, 2001;Tang et al, 2002) whereas C57BL/6J mice show an intermediate phenotype in most behaviors (Crawley, 1999) and are often used in strain comparisons. Moreover, mice display greater changes in REM than in NREM after exposure to novelty (Tang et al, 2004; and after experiencing stressors such as fearful stimuli (Sanford et al, 2001;Sanford et al, 2003a;2003b;2003d;Liu et al, 2004) and restraint (Wurbel et al, 1998;Meerlo et al, 2001;Liu et al, 2004). The relative magnitude and duration of the changes in sleep has been found to vary with strain.…”

Section: Introductionmentioning

confidence: 99%

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Mouse strain differences in the effects of corticotropin releasing hormone (CRH) on sleep and wakefulness

et al. 2008

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Corticotropin releasing hormone (CRH) plays a major role in central nervous system responses to stressors and has been implicated in stress-induced alterations in sleep. In the absence of stressors, CRH contributes to the regulation of spontaneous waking. We examined the effects of CRH and astressin (AST), a non-specific CRH antagonist, on wakefulness and sleep in two mouse strains with differential responsiveness to stress to determine whether CRH might also differentially affect undisturbed sleep and activity. Less reactive C57BL/6J (n=7) and high reactive BALB/cJ (n=7) male mice were implanted with a transmitter for determining sleep via telemetry and with a guide cannula aimed into a lateral ventricle. After recovery from surgery and habituation to handling, ICV microinjections of CRH (0.04, 0.2, and 0.4 μg), AST (0.1, 0.4, and 1.0 μg) or vehicle alone (pyrogenfree saline, 0.2 μl) were administered during the fourth h after lights on and sleep was recorded for the subsequent 8 h. Comparisons of wakefulness and sleep were conducted across conditions and across strains. In C57BL/6J mice, REM was significantly decreased after microinjections of CRH (0.2 μg) and CRH (0.4 μg), and NREM and total sleep were decreased after microinjections of CRH (0.4 μg ). CRH (0.4 μg) and AST did not significantly change wakefulness or sleep. In BALB/cJ mice, CRH (0.4 μg) increased wakefulness and decreased NREM, REM and total sleep. AST decreased active wakefulness and significantly increased REM at the low and high dosages. These findings demonstrate that CRH produces changes in arousal when given to otherwise undisturbed mice. Strain differences in the effects of CRH and AST may be linked to the relative responsiveness of C57BL/6J and BALB/cJ mice to stressors and to underlying differences in the CRH system.

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Section: Discussionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 61%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Mouse strain differences in the effects of corticotropin releasing hormone (CRH) on sleep and wakefulness

et al. 2008

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“…GABAergic and cholinergic transmission interact in the pontine reticular formation to regulate sleep and wakefulness (Vazquez and Baghdoyan, 2004). Microinjection data from cat (Xi et al, 1999), rat (Sanford et al, 2003), and mouse (Chang et al, 2005, Chang et al, 2006 concur in showing that GABAergic transmission in the pontine reticular formation promotes wakefulness. Therefore, the present study was designed to test the hypothesis that μ-opioid receptors in the oral portion of rat pontine reticular formation (PnO) modulate PnO GABA levels.…”

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confidence: 99%

Sleep and GABA levels in the oral part of rat pontine reticular formation are decreased by local and systemic administration of morphine

2007

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Morphine, a μ-opioid receptor agonist, is a commonly prescribed treatment for pain. Although highly efficacious, morphine has many unwanted side effects including disruption of sleep and obtundation of wakefulness. One mechanism by which morphine alters sleep and wakefulness may be by modulating GABAergic signaling in brain regions regulating arousal, including the oral pontine reticular formation (PnO). This study used in vivo microdialysis in unanesthetized Sprague-Dawley rat to test the hypothesis that μ-opioid receptors modulate PnO GABA levels. Validation of the high performance liquid chromatographic technique used to quantify GABA was obtained by dialyzing the PnO (n=4 rats) with the GABA reuptake inhibitor nipecotic acid (500 μM). Nipecotic acid caused a 185±20% increase in PnO GABA levels, confirming chromatographic detection of GABA and demonstrating the existence of functional GABA transporters in rat PnO. Morphine caused a concentration-dependent decrease in PnO GABA levels (n=25 rats). Coadministration of morphine (100 μM) with naloxone (1 μM), a μ-opioid receptor antagonist, blocked the morphine-induced decrease in PnO GABA levels (n=5 rats). These results show for the first time that μ-opioid receptors in rat PnO modulate GABA levels. A second group of rats (n=6) was used to test the hypothesis that systemically administered morphine also decreases PnO GABA levels. Intravenous morphine caused a significant (p<0.05) decrease (19%) in PnO GABA levels relative to control intravenous infusions of saline. Finally, microinjections followed by 2 h recordings of electroencephalogram and electromyogram tested the hypothesis that PnO morphine administration disrupts sleep (n=8 rats). Morphine significantly (p<0.05) increased the percent of time spent in wakefulness (65%) and significantly (p<0.05) decreased the percent of rapid eye movement (REM) sleep (-53%) and non-REM sleep (-69%). The neurochemical and behavioral data suggest that morphine may disrupt sleep, at least in part, by decreasing GABAergic transmission in the PnO. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2009 August 20. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptOpioids such as morphine, that exert their effects primarily via the μ-opioid receptor, are the most efficacious and widely prescribed treatments for pain (Yaksh, 1997, Nicholson, 2003. Unfortunately, opioids have numerous side effects including sleep disruption (Kay et al., 1969, Kay, 1975. In healthy human voluntee...

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Movement suppression during anesthesia: Neural projections from the mesopontine tegmentum to areas involved in motor control

Sukhotinsky

Hopkins

Lü

et al. 2005

J of Comparative Neurology

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Microinjection of pentobarbital and GABA(A)-receptor agonists into a brainstem region we have called the mesopontine tegmental anesthesia area (MPTA; Devor and Zalkind [2001] Pain 94:101-112) induces a general anesthesia-like state. As in systemic general anesthesia, rats show loss of the righting reflex, atonia, nonresponsiveness to noxious stimuli, and apparent loss of consciousness. GABA(A) agonist anesthetics acting on the MPTA might suppress movement by engaging endogenous motor regulatory systems previously identified in research on decerebrate rigidity and REM sleep atonia. Anterograde and retrograde tracing revealed that the MPTA has multiple descending projections to pontine and medullary areas known to be associated with motor control and atonia. Prominent among these are the dorsal pontine reticular formation and components of the rostral ventromedial medulla (RVM). The MPTA also has direct projections to the intermediate gray matter and ventral horn of the spinal cord via the lateral and anterior funiculi. These projections show a rostrocaudal topography: neurons in the rostral MPTA project to the RVM, but only minimally to the spinal cord, while those in the caudal MPTA project to both targets. Finally, the MPTA has ascending projections to motor control areas including the substantia nigra, subthalamic nucleus, and the caudate-putamen. Projections are bilateral with an ipsilateral predominance. We propose that GABA(A) agonist anesthetics induce immobility at least in part by acting on these endogenous motor control pathways via the MPTA. Analysis of MPTA connectivity has the potential for furthering our understanding of the neural circuitry responsible for the various functional components of general anesthesia.

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GABAergic Regulation of REM Sleep in Reticularis Pontis Oralis and Caudalis in Rats

Cited by 82 publications

References 20 publications

Mouse strain differences in the effects of corticotropin releasing hormone (CRH) on sleep and wakefulness

Mouse strain differences in the effects of corticotropin releasing hormone (CRH) on sleep and wakefulness

Sleep and GABA levels in the oral part of rat pontine reticular formation are decreased by local and systemic administration of morphine

Movement suppression during anesthesia: Neural projections from the mesopontine tegmentum to areas involved in motor control

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