Rêve et schizophrénie : Un même support neurobiologique ?

L’activité mentale de l’éveil est tributaire de processus centraux à la fois antagonistes et complémentaires. En effet, au niveau cortical, agissent conjointement des neuromédiateurs activateurs - acétylcholine et glutamate - et d’autres essentiellement inhibiteurs tels que GABA, noradrénaline et sérotonine. Pendant le sommeil paradoxal, les taux des deux derniers chutent drastiquement, ce qui pourrait entraîner, directement ou indirectement, la désorganisation des structures corticales et sous corticales, les anomalies de l’excitabilité centrale, ainsi que la baisse du flux sanguin dans le cortex préfrontal dorsolatéral. Ces dysfonctionnements s’observent à la fois chez le schizophrène et pendant le sommeil paradoxal chez le sujet normal. De plus, la baisse de la dopamine dans le cortex préfrontal en sommeil paradoxal, mise en évidence par l’expérimentation animale, permet à présent d’établir un lien de cause à effet entre ce déficit dopaminergique et l’altération du jugement critique rencontrée tant dans le rêve que dans la schizophrénie. Dans le noyau accumbens, l’augmentation de dopamine et la diminution concomitante du glutamate expliqueraient l’activité hallucinatoire et délirante du rêve et de la schizophrénie. Sommeil paradoxal et schizophrénie partageant les mêmes caractéristiques psychologiques, électrophysiologiques, circulatoires, pharmacologiques et neurochimiques, cette phase de sommeil pourrait constituer un bon modèle neurobiologique de cette maladie mentale.Normal waking mentation is the outcome of the combined action of both electrophysiological and neurochemical antagonistic and complementary activating and inhibitory influences occurring mainly in the cerebral cortex. The chemical ones are supported principally by acetylcholine, and noradrenaline and serotonin, respectively. During rapid eye movement (REM) sleep, the monoaminergic silence - except dopaminergic ongoing activity - disrupts this equilibrium and seems to be responsible for disturbances of mental activity characteristic of dreaming. This imbalance could cause disconnectivity of cortical areas, failure of latent inhibition and possibly the concomitant prefrontal dorsolateral deactivation. Moreover, the decrease of prefrontal dopaminergic functioning could explain the loss of reflectiveness in this sleep stage. All these phenomena are also encountered in schizophrenia. The psychotic-like mentation of dreaming (hallucinations, delusions, bizarre thought processes) could result from the disinhibition of dopamine influence in the nucleus accumbens by the noradrenergic and serotonergic local silence and/or the lifting of glutamate influence from the prefrontal cortex and hippocampus. We hypothesize that, during REM sleep, the increase of dopamine and the decrease of glutamate release observed in nucleus accumbens reach the threshold values at which psychotic disturbances arise during wakefulness. Whatever the precise mechanism, it seems that the functional state of the prefrontal cortex and nucleus accumbens is the same during dreaming sleep stage and in schizophrenia. The convergent psychological, electrophysiological, tomographic, pharmacological and neurochemical criteria of REM sleep and schizophrenia suggest that this sleep stage could become a good neurobiological model of this psychiatric disease

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The existence of spacetime singularities is irrelevant for the irreversible appearance of black holes. However, confirmation of the latter's unitary dynamics would require the preparation of a coherent superposition of a tremendous number of appropriate ``Everett worlds''.Comment: 10 pages, 1 figure, Latex - Invited paper for a special Einstein issue of Physics Letters

Linear optics implementation of general two-photon projective measurement

We will present a method of implementation of general projective measurement of two-photon polarization state with the use of linear optics elements only. The scheme presented succeeds with a probability of at least 1/16. For some specific measurements, (e.g. parity measurement) this probability reaches 1/4.Comment: 8 page

The Involvement of Noradrenaline in Rapid Eye Movement Sleep Mentation

Noradrenaline, one of the main brain monoamines, has powerful central influences on forebrain neurobiological processes which support the mental activities occurring during the sleep–waking cycle. Noradrenergic neurons are activated during waking, decrease their firing rate during slow wave sleep, and become silent during rapid eye movement (REM) sleep. Although a low level of noradrenaline is still maintained during REM sleep because of diffuse extrasynaptic release without rapid withdrawal, the decrease observed during REM sleep contributes to the mentation disturbances that occur during dreaming, which principally resemble symptoms of schizophrenia but seemingly also of attention deficit hyperactivity disorder

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

Emerging pharmacotherapy for cancer patients with cognitive dysfunction

Advances in the diagnosis and multi-modality treatment of cancer have increased survival rates for many cancer types leading to an increasing load of long-term sequelae of therapy, including that of cognitive dysfunction. The cytotoxic nature of chemotherapeutic agents may also reduce neurogenesis, a key component of the physiology of memory and cognition, with ramifications for the patient's mood and other cognition disorders. Similarly radiotherapy employed as a therapeutic or prophylactic tool in the treatment of primary or metastatic disease may significantly affect cognition. A number of emerging pharmacotherapies are under investigation for the treatment of cognitive dysfunction experienced by cancer patients. Recent data from clinical trials is reviewed involving the stimulants modafinil and methylphenidate, mood stabiliser lithium, anti-Alzheimer's drugs memantine and donepezil, as well as other agents which are currently being explored within dementia, animal, and cell culture models to evaluate their use in treating cognitive dysfunction

Structural and functional analysis of the E. coli NusB-S10 transcription antitermination complex.

Protein S10 is a component of the 30S ribosomal subunit and participates together with NusB protein in processive transcription antitermination. The molecular mechanisms by which S10 can act as a translation or a transcription factor are not understood. We used complementation assays and recombineering to delineate regions of S10 dispensable for antitermination, and determined the crystal structure of a transcriptionally active NusB-S10 complex. In this complex, S10 adopts the same fold as in the 30S subunit and is blocked from simultaneous association with the ribosome. Mass spectrometric mapping of UV-induced crosslinks revealed that the NusB-S10 complex presents an intermolecular, composite and contiguous binding surface for RNAs containing BoxA antitermination signals. Furthermore, S10 overproduction complemented a nusB null phenotype. These data demonstrate that S10 and NusB together form a BoxA-binding module; that NusB facilitates entry of S10 into the transcription machinery; and that S10 represents a central hub in processive antitermination

Effects of oral gamma-aminobutyric acid (GABA) administration on stress and sleep in humans: a systematic review

Gamma-aminobutyric acid (GABA) is a non-proteinogenic amino acid and is the main inhibitory neurotransmitter in the mammalian brain. GABA's stress-reducing, and sleep enhancing effects have been established. However, although several human clinical trials have been conducted, results regarding the role of natural and/or biosynthetic oral GABA intake on stress and sleep are mixed. We performed a systematic review to examine whether natural and/or biosynthetic oral GABA intake has an effect on stress and sleep. We systematically searched on PubMed database for studies published up to February 2020 following PRISMA guidelines. Only placebo-controlled human trials that assessed stress, sleep, and related psychophysiological outcomes as a response to natural GABA (i.e., GABA that is present naturally in foods) or biosynthetic GABA (i.e., GABA that is produced via fermentation) intake were included. Fourteen studies met the criteria and were included in the systematic review. Although more studies are needed before any inferences can be made about the efficacy of oral GABA consumption on stress and sleep, results show that there is limited evidence for stress and very limited evidence for sleep benefits of oral GABA intake

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