REM sleep: A biological and psychological paradox

Brain Research Institute, UCLA, Los Angeles, CA 90095, USA
Sleep Medicine Reviews (Impact Factor: 8.51). 06/2011; 15(3):139-42. DOI: 10.1016/j.smrv.2011.01.001
Source: PubMed
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    • "The biological function of REM sleep still remains a mystery (Siegel 2011), although several theories have been advanced (Hobson 2009; Horne 2000; Horne 2013; Roffwarg and others 1966; Siegel 2005). According to one theory, when the brain is isolated from external inputs during REM sleep, random patterns of activation can be generated that are useful for elimination of " parasitic modes " of activity (Crick and Mitchison 1983). "
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    ABSTRACT: The overall function of sleep is hypothesized to provide "recovery" after preceding waking activities, thereby ensuring optimal functioning during subsequent wakefulness. However, the functional significance of the temporal dynamics of sleep, manifested in the slow homeostatic process and the alternation between non-rapid eye movement (NREM) and REM sleep remains unclear. We propose that NREM and REM sleep have distinct and complementary contributions to the overall function of sleep. Specifically, we suggest that cortical slow oscillations, occurring within specific functionally interconnected neuronal networks during NREM sleep, enable information processing, synaptic plasticity, and prophylactic cellular maintenance ("recovery process"). In turn, periodic excursions into an activated brain state-REM sleep-appear to be ideally placed to perform "selection" of brain networks, which have benefited from the process of "recovery," based on their offline performance. Such two-stage modus operandi of the sleep process would ensure that its functions are fulfilled according to the current need and in the shortest time possible. Our hypothesis accounts for the overall architecture of normal sleep and opens up new perspectives for understanding pathological conditions associated with abnormal sleep patterns.
    The Neuroscientist 03/2014; 20(3). DOI:10.1177/1073858413518152 · 6.84 Impact Factor
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    • "Sleep is controlled by a series of neurotransmitters including serotonin and acetylcholine which are produced from their amino acid precursors tryptophan and choline. Cycling neurotransmitters determine the sleep stages including phase IV delta and REM sleep.13–19 Adequate production and timely release of these neurotransmitters are necessary for the production of sleep cycles. "
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    ABSTRACT: Sleep disorders are a common and poorly treated disease state. This double blind, four arm placebo-controlled, randomized trial compared (1) low dose trazodone, (2) Sentra PM, a neurotransmitter based medical food, (3) the joint administration of trazodone and the medical food Sentra PM and (4) placebo. There were 111 subjects studied in 12 independent sites. Subjects underwent baseline screening, informed consent and an initial sleep questionnaire. After 14 days subjects underwent a second evaluation by questionnaire. At baseline and Day 14 the subjects underwent 24 hour ECG recordings that were analyzed in the frequency domain of heart rate variability. The specific high frequency parasympathetic autonomic nervous system activity was analyzed. The primary endpoints were sleep latency and parasympathetic autonomic nervous system improvement in sleeping hours. The results showed improvement in sleep latency for the Sentra PM and combination of Sentra PM and trazodone (-41 and -56 minutes P < 0.001). There was an improvement in quality of sleep for the amino acid formulation Sentra PM and the combination (3.86 and 6.48 Likert units on a 10 point scale P < 0.001). There was an activation of circadian activity percent at night in the medical food and combination groups while there was no change in parasympathetic activity in either the placebo or trazodone group. These data indicate that Sentra PM can improve the quality of sleep, the response to trazodone as a sleep medication and parasympathetic autonomic nervous system activity.
    04/2012; 4:65-72. DOI:10.4137/JCNSD.S9381
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    • "Lesions of the SCN abolish circadian rhythmicity for sleep and other biological processes (Moore and Eichler, 1972; Stephan and Zucker, 1972; Eastman et al., 1984; Edgar et al., 1993; Mistlberger, 2005; Kohsaka and Bass, 2007). While the SCN signals the timing of sleep–wake cycles, an intricate neurocircuitry consisting of neurochemically distinct nuclei residing in the basal forebrain, preoptic area, lateral hypothalamus, and brainstem is responsible for the induction and maintenance of arousal and the different sleep stages, rapid eye movement sleep (REMS) and non-REMS (for review, see Jones, 2005; Saper et al., 2005; Szymusiak and McGinty, 2008; Saper et al., 2010; Siegel, 2011). The SCN and sleep–wake neurocircuits are anatomically linked (Chou et al., 2002, 2003; Deurveilher et al., 2002; Deurveilher and Semba, 2003, 2005), and neurobiological research over the past 30 years clearly points to an interaction between homeostatic and circadian processes in the regulation of sleep–wake cycles (for review, see Mistlberger , 2005; Saper et al., 2005; Franken and Dijk, 2009; Rosenwasser, 2009). "
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    ABSTRACT: While much is known about the mechanisms that underlie sleep and circadian rhythms, the investigation into sex differences and gonadal steroid modulation of sleep and biological rhythms is in its infancy. There is a growing recognition of sex disparities in sleep and rhythm disorders. Understanding how neuroendocrine mediators and sex differences influence sleep and biological rhythms is central to advancing our understanding of sleep-related disorders. While it is known that ovarian steroids affect circadian rhythms in rodents, the role of androgen is less understood. Surprising findings that androgens, acting via androgen receptors in the master "circadian clock" within the suprachiasmatic nucleus, modulate photic effects on activity in males point to novel mechanisms of circadian control. Work in aromatase-deficient mice suggests that some sex differences in photic responsiveness are independent of gonadal hormone effects during development. In parallel, aspects of sex differences in sleep are also reported to be independent of gonadal steroids and may involve sex chromosome complement. This a summary of recent work illustrating how sex differences and gonadal hormones influence sleep and circadian rhythms that was presented at a Mini-Symposium at the 2011 annual meeting of the Society for Neuroscience.
    The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 11/2011; 31(45):16107-16. DOI:10.1523/JNEUROSCI.4175-11.2011 · 6.34 Impact Factor
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