Neurobiological mechanisms for the regulation of mammalian sleep–wake behavior: Reinterpretation of historical evidence and inclusion of contemporary cellular and molecular evidence

Datta, Subimal; MacLean, R. Ross

doi:10.1016/j.neubiorev.2007.02.004

Cited by 268 publications

(259 citation statements)

References 667 publications

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“…To our knowledge, this is the first work exploring the association of brain volumes and saccade velocity in SCA2. Besides, the degeneration of the pontine brainstem in SCA2 is in line with the early REM sleep pathology characterizing the disease from prodromal to manifest stage35, 36, 37 since the neural circuit controlling this sleep stage lie mainly in the pontine brainstem 38, 39…”

Section: Discussionmentioning

confidence: 70%

Brain atrophy measures in preclinical and manifest spinocerebellar ataxia type 2

Reetz

Rodríguez‐Labrada²,

Dogan

et al. 2018

Ann Clin Transl Neurol

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ObjectiveSpinocerebellar ataxia type 2 (SCA2) is an autosomal dominantly inherited neurodegenerative disease mainly affecting the cerebellum and brainstem. In this Cuban‐German research collaboration, we aimed to characterize atrophy patterns and associations with clinical measures in preclinical and manifest SCA2.MethodsIn this study, 16 nonmanifest SCA2 mutation carriers, 26 manifest patients with SCA2, and 18 healthy control subjects underwent magnetic resonance imaging, as well as genetic and clinical characterization including assessment of ataxia (Scale for the Assessment and Rating of Ataxia) and saccade velocity in Cuba were enrolled. Semiautomated quantitative volumetry of the cerebellum and brainstem, subdivided into the medulla oblongata, the pontine brainstem, and mesencephalon was performed. Additionally, the anteroposterior diameter of the pontine brainstem was measured.ResultsAnalysis of volumetric data revealed degeneration of the cerebellum and brainstem, in particular of pontine volumes and the anteroposterior diameter of the pons, in both manifest SCA2 patients and individuals at risk for SCA2 compared to controls. Comparing patients with nonataxic preclinical SCA2 mutation carriers, we found more pronounced reductions of the pontine brainstem and cerebellum in manifest SCA2. Volumetric data further showed associations with CAG repeat length and predicted age of onset in preclinical SCA2 individuals, and by trend with ataxia signs in patients. Although saccade velocity was associated with reduction in the pontine brainstem in preclinical and manifest SCA2, reduced ability to suppress interfering stimuli measured by the Stroop task was related to cerebellar volume loss in patients.InterpretationPreclinical SCA2 mutation carriers exhibit brain abnormalities, which could be targeted as surrogate parameters for disease progression and in future preventive trials.

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Section: Discussionmentioning

confidence: 70%

Brain atrophy measures in preclinical and manifest spinocerebellar ataxia type 2

Reetz

Rodríguez‐Labrada²,

Dogan

et al. 2018

Ann Clin Transl Neurol

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“…In conclusion, while further studies especially bilateral infusion of THIP in the PFH and other wakefulness centers (Datta and Maclean, 2007) and monitoring the effects of THIP during the dark period are necessary; our initial study suggests that unilateral perfusion of THIP, a selective extrasynaptic GABA A receptor agonist, into the orexinergic PFH increased nonREM sleep and reduced wakefulness during the light period in freely behaving, naturally sleeping rats. This is the first study to implicate extrasynaptic GABA A receptors in the orexinergic PFH in the control of sleep-wakefulness and the first to localize the effects of THIP to a specific brain region in freely behaving rats.…”

Section: Discussionmentioning

confidence: 74%

Effect of microdialysis perfusion of 4,5,6,7-tetrahydroisoxazolo-[5,4-c]pyridine-3-ol in the perifornical hypothalamus on sleep–wakefulness: Role of δ-subunit containing extrasynaptic GABAA receptors

2008

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Gaboxadol or 4,5,6,7-tetrahydroisoxazolo-[5,4-c]pyridine-3-ol (THIP) is a selective agonist for the δ-subunit containing extrasynaptic GABA A receptors that will soon enter the U.S. market as a sleep aid (Winsky-Sommerer et al., 2007). Numerous studies have shown that systemic administration of THIP reduces wakefulness and increases sleep both in humans and rats (Lancel and Langebartels, 2000;Walsh et al., 2007). However, it is yet unclear where in the brain THIP acts to promote sleep. Since the perifornical lateral hypothalamus (PFH) contains orexin neurons and orexin neurons are critical for maintenance of arousal (McCarley, 2007), we hypothesized that THIP may act on PFH neurons to promote sleep. To test our hypothesis, we used reverse microdialysis to perfuse THIP unilaterally into the PFH and studied its effects on sleep-wakefulness during the light period in freely behaving rats. Microdialysis perfusion of THIP (100 µM) into the PFH produced a significant reduction in wakefulness with a concomitant increase in nonREM sleep as compared to ACSF perfusion. REM sleep was unaffected. This is the first study implicating the δ-subunit containing extrasynaptic GABA A receptors in PFH in control of sleep-wakefulness in freely behaving rats. KeywordsOrexin/hypocretin; perifornical hypothalamus; THIP; reverse microdialysisThe γ-aminobutyric acid (GABA) system is closely linked with the regulation of sleepwakefulness. Thus, it is not surprising that pharmacological landscape for treatment of various sleep disorders including insomnia have been dominated by agents that activate GABA A receptors . Classical synaptic GABA transmission results in phasic inhibition that is mainly mediated by γ2 subunits containing postsynaptic GABA A receptors (Rudolph and Mohler, 2006;Ebert et al., 2006;Olsen et al., 2007), In contrast, tonic inhibition is mainly mediated by δ subunit containing "extrasynaptic" GABA A receptors (Olsen et al.,Correspondence: Mahesh Thakkar, Harry Truman Memorial Veteran's Hospital, Columbia, MO., Department of Neurology, University of Missouri, 800 Hospital Drive, Columbia, MO, 65201, Ph. (573) 814 6000 ext 53697, Email: thakkarmm@health.missouri.edu. 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. 2007). These "extrasynaptic" GABA A receptors have a higher affinity for GABA and slower rates of desensitization and deactivation than do the classical synaptic receptors. NIH Public AccessThe GABA A agonist THIP selectively activates extrasynaptic GABA A receptors (WinskySommerer et al., 2007). Systemic administration of THIP induces sleep in rats and humans (...

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“…Similarly, normal sleep is also critical for psychological and emotional well-being (reviewed in Datta and Maclean, 2007). Thus, evaluating changes in sleep-wake behavior in after stressor exposure could elucidate diagnostic criteria and symptoms for specific disorders.…”

Section: Discussionmentioning

confidence: 99%

The relationship between anxiety and sleep–wake behavior after stressor exposure in the rat

MacLean

Datta

2007

Brain Research

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Disturbed sleep is a common subjective complaint among individuals diagnosed with anxiety disorders. In rodents, sleep is often recorded after exposure to various foot-shock paradigms designed to induce an anxiety state. Although differences in sleep-wake architecture are noted, the relationship to specific level of anxiety is often assumed or absent. Utilizing the elevated plus maze (EPM) after exposure to escapable shock (ES), inescapable shock (IS) or fear conditioning (FC), resulting differences in sleep architecture were compared to an objective measure of anxiety. Male Wistar rats were implanted with EEG, EMG and hippocampal theta electrodes to record sleep-wake behavior. After recovery and recording of baseline sleep, rats were exposed to one of five manipulations: ES, IS, FC, or control (CES or CIS; utilizing either chamber with no shock exposure). Shortly after experimental manipulation, the EPM was employed to quantify traditional and ethological measures of anxiety and polygraphic signs of sleep-wake behavior were recorded continuously for 6h. Although no significance was observed in EPM measurements across groups, profound differences in sleep architecture were present. Individual correlation analysis revealed no differences in anxiety level and total percentage of time spent in sleep-wake states. These results indicate that differences in sleep architecture after foot-shock exposure may not be simply due to increased anxiety. Rather, individual anxiety may be exacerbated by disrupted sleep. To fully understand the relationship between anxiety and sleep-wake behavior, a more objective analysis of anxiety after stressor exposure is mandated.

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Neurobiological mechanisms for the regulation of mammalian sleep–wake behavior: Reinterpretation of historical evidence and inclusion of contemporary cellular and molecular evidence

Cited by 268 publications

References 667 publications

Brain atrophy measures in preclinical and manifest spinocerebellar ataxia type 2

Brain atrophy measures in preclinical and manifest spinocerebellar ataxia type 2

Effect of microdialysis perfusion of 4,5,6,7-tetrahydroisoxazolo-[5,4-c]pyridine-3-ol in the perifornical hypothalamus on sleep–wakefulness: Role of δ-subunit containing extrasynaptic GABAA receptors

The relationship between anxiety and sleep–wake behavior after stressor exposure in the rat

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