Selective Rapid Eye Movement Sleep Deprivation Affects Cell Size and Number in Kitten Locus Coeruleus

Cells in the locus coeruleus (LC) constitute the sole source of norepinephrine (NE) in the brain and change their discharge rates according to vigilance state. In addition to its well established role in vigilance, NE affects synaptic plasticity in the postnatal critical period (CP) of development. One form of CP synaptic plasticity affected by NE results from monocular occlusion, which leads to physiological and cytoarchitectural alterations in central visual areas. Selective suppression of rapid eye movement sleep (REMS) in the CP kitten enhances the central effects of monocular occlusion. The mechanisms responsible for heightened cortical plasticity following REMS deprivation (REMSD) remain undetermined. One possible mediator of an increase in plasticity is continuous NE outflow, which presumably persists during extended periods of REMSD. Tyrosine hydroxylase (TH) is the rate-limiting enzyme in the synthesis of NE and serves as a marker for NE-producing cells. We selectively suppressed REMS in kittens for 1 week during the CP. The number and size of LC cells expressing immunoreactivity to tyrosine hydroxylase (TH-ir) was assessed in age-matched REMS-deprived (RD)-, treatment–control (TXC)-, and home cage-reared (HCC) animals. Sleep amounts and slow wave activity (SWA) were also examined relative to baseline. Time spent in REMS during the study was lower in RD compared to TXC animals, and RD kittens increased SWA delta power in the latter half of the REMSD period. The estimated total number of TH-ir cells in LC was significantly lower in the RD than in the TXC kittens and numerically lower than in the HCC animals. The size of LC cells expressing TH-ir was greatest in the HCC group. HCC cells were significantly larger than TH-ir cells in the RD kittens. These data are consistent with presumed reduction in NE in forebrain areas, including visual cortex, caused by 1 week of REMSD

Sleep Disorders and Genes

Versão preprintThe sleep-wake cycle is a neurobiological phenomenon that shows intervals of activity alternating with restfulness that appears with a periodicity approximating the 24h day-night cycle. The sleep-wake cycle is under the control of diverse neuroanatomical and neurochemical systems, including monoaminergic, cholinergic, adenosinergic among many other systems. In addition, neuroanatomical centers linked to sleep promotion, such as hypothalamus, project to the cerebral cortex, subcortical relays and brainstem. In addition, the sleep-wake cycle has been associated to aberrant features known as sleep disorders. Here, we will discuss the role of specific gene expression on sleep disturbances. Given the expansion of the knowledge in the sleep-wake cycle area, it is indeed ambitious to describe all the genetics involved in the sleep modulation. However, in this chapter we reviewed the current understanding of the sleep disorders and gene expression.info:eu-repo/semantics/publishedVersio

The Neural Substrates of Infant Sleep in Rats

Sleep is a poorly understood behavior that predominates during infancy but is studied almost exclusively in adults. One perceived impediment to investigations of sleep early in ontogeny is the absence of state-dependent neocortical activity. Nonetheless, in infant rats, sleep is reliably characterized by the presence of tonic (i.e., muscle atonia) and phasic (i.e., myoclonic twitching) components; the neural circuitry underlying these components, however, is unknown. Recently, we described a medullary inhibitory area (MIA) in week-old rats that is necessary but not sufficient for the normal expression of atonia. Here we report that the infant MIA receives projections from areas containing neurons that exhibit state-dependent activity. Specifically, neurons within these areas, including the subcoeruleus (SubLC), pontis oralis (PO), and dorsolateral pontine tegmentum (DLPT), exhibit discharge profiles that suggest causal roles in the modulation of muscle tone and the production of myoclonic twitches. Indeed, lesions in the SubLC and PO decreased the expression of muscle atonia without affecting twitching (resulting in “REM sleep without atonia”), whereas lesions of the DLPT increased the expression of atonia while decreasing the amount of twitching. Thus, the neural substrates of infant sleep are strikingly similar to those of adults, a surprising finding in light of theories that discount the contribution of supraspinal neural elements to sleep before the onset of state-dependent neocortical activity

Does Sleep Improve Your Grammar? : Preferential Consolidation of Arbitrary Components of New Linguistic Knowledge

We examined the role of sleep-related memory consolidation processes in learning new form-meaning mappings. Specifically, we examined a Complementary Learning Systems account, which implies that sleep-related consolidation should be more beneficial for new hippocampally dependent arbitrary mappings (e.g. new vocabulary items) relative to new systematic mappings (e.g. grammatical regularities), which can be better encoded neocortically. The hypothesis was tested using a novel language with an artificial grammatical gender system. Stem-referent mappings implemented arbitrary aspects of the new language, and determiner/suffix+natural gender mappings implemented systematic aspects (e.g. tib scoiffesh + ballerina, tib mofeem + bride; ked jorool + cowboy, ked heefaff + priest). Importantly, the determiner-gender and the suffix-gender mappings varied in complexity and salience, thus providing a range of opportunities to detect beneficial effects of sleep for this type of mapping. Participants were trained on the new language using a word-picture matching task, and were tested after a 2-hour delay which included sleep or wakefulness. Participants in the sleep group outperformed participants in the wake group on tests assessing memory for the arbitrary aspects of the new mappings (individual vocabulary items), whereas we saw no evidence of a sleep benefit in any of the tests assessing memory for the systematic aspects of the new mappings: Participants in both groups extracted the salient determiner-natural gender mapping, but not the more complex suffix-natural gender mapping. The data support the predictions of the complementary systems account and highlight the importance of the arbitrariness/systematicity dimension in the consolidation process for declarative memories

Rapid Eye Movements in Sleep Furnish a Unique Probe Into Consciousness

The neural correlates of rapid eye movements (REMs) in sleep are extraordinarily robust; including REM-locked multisensory-motor integration and accompanying activation in the retrosplenial cortex, the supplementary eye field and areas encompassing cholinergic basal nucleus (Hong et al., 2009). The phenomenology of REMs speaks to the notion that perceptual experience in both sleep and wakefulness is a constructive process – in which we generate predictions of sensory inputs and then test those predictions through actively sampling the sensorium with eye movements. On this view, REMs during sleep may index an internalized active sampling or ‘scanning’ of selfgenerated visual constructs that are released from the constraints of visual input. If this view is correct, it renders REMs an ideal probe to study consciousness as “an exclusively internal affair” (Metzinger, 2009). In other words, REMs offer a probe of active inference – in the sense of predictive coding – when the brain is isolated from the sensorium in virtue of the natural blockade of sensory afferents during REM sleep. Crucially, REMs are temporally precise events that enable powerful inferences based on time series analyses. As a natural, task-free probe, (REMs) could be used in non-compliant subjects, including infants and animals. In short, REMs constitute a promising probe to study the ontogenetic and phylogenetic development of consciousness and perhaps the psychopathology of schizophrenia and autism, which have been considered in terms of aberrant predictive coding

Annual Research Review: Sleep problems in childhood psychiatric disorders – a review of the latest science

Background Hippocrates flagged the value of sleep for good health. Nonetheless, historically, researchers with an interest in developmental psychopathology have largely ignored a possible role for atypical sleep. Recently, however, there has been a surge of interest in this area, perhaps reflecting increased evidence that disturbed or insufficient sleep can result in poor functioning in numerous domains. This review outlines what is known about sleep in the psychiatric diagnoses most relevant to children and for which associations with sleep are beginning to be understood. While based on a comprehensive survey of the literature, the focus of the current review is on the latest science (largely from 2010). There is a description of both concurrent and longitudinal links as well as possible mechanisms underlying associations. Preliminary treatment research is also considered which suggests that treating sleep difficulties may result in improvements in behavioural areas beyond sleep quality. Findings To maximise progress in this field, there now needs to be: (a) greater attention to the assessment of sleep in children; (b) sleep research on a wider range of psychiatric disorders; (c) a greater focus on and examination of mechanisms underlying associations; (d) a clearer consideration ofdevelopmental questions and (e) large-scale well-designed treatment studies. Conclusions While sleep problems may sometimes be missed by parents and healthcare providers; hence constituting a hidden risk for other psychopathologies – knowing about these difficulties creates unique opportunities. The current excitement in this field from experts in diverse areas including developmental psychology, clinical psychology, genetics and neuropsychology should make these opportunities a reality