Dietary Zinc Acts as a Sleep Modulator

While zinc is known to be important for many biological processes in animals at a molecular and physiological level, new evidence indicates that it may also be involved in the regulation of sleep. Recent research has concluded that zinc serum concentration varies with the amount of sleep, while orally administered zinc increases the amount and the quality of sleep in mice and humans. In this review, we provide an exhaustive study of the literature connecting zinc and sleep, and try to evaluate which molecular mechanism is likely to be involved in this phenomenon. A better understanding should provide critical information not only about the way zinc is related to sleep but also about how sleep itself works and what its real function is

Nonlinear terahertz control of the lead halide perovskite lattice

Lead halide perovskites (LHPs) have emerged as an excellent class of semiconductors for next-generation solar cells and optoelectronic devices. Tailoring physical properties by fine-tuning the lattice structures has been explored in these materials by chemical composition or morphology. Nevertheless, its dynamic counterpart, phonon-driven ultrafast material control, as contemporarily harnessed for oxide perovskites, has not yet been established. Here, we use intense THz electric fields to obtain direct lattice control via nonlinear excitation of coherent octahedral twist modes in hybrid CH3NH3PbBr3 and all-inorganic CsPbBr3 perovskites. These Raman-active phonons at 0.9 to 1.3 THz are found to govern the ultrafast THz-induced Kerr effect in the low-temperature orthorhombic phase and thus dominate the phonon-modulated polarizability with potential implications for dynamic charge carrier screening beyond the Fröhlich polaron. Our work opens the door to selective control of LHP’s vibrational degrees of freedom governing phase transitions and dynamic disorder

ADAPTATION CELLULAIRE À LA DISPONIBILITÉ DES ACIDES AMINÉS : MÉCANISMES IMPLIQUÉS DANS LA RÉGULATION DE L’EXPRESSION DES GÈNES

In mammals, the impact of nutrients on gene expression has become an important area of research. Nevertheless, the current understanding of amino acid-dependent control of gene expression is limited. Amino acids have multiple and important functions, so their homeostasis has to be finely maintained. However, the amino acidemia can be affected by certain nutritional conditions or various forms of aggression. It follows that mammals have to adjust several of their physiological functions involved in the adaptation to amino acid availability by regulating expression of numerous genes. The aim of this review is to examine the role of amino acids in regulating mammalian gene expression and physiological functions. A limitation for several amino acids strongly increases the expression of target genes such as IGFBP-1, CHOP and asparagine synthetase (AS) genes. The molecular mechanisms involved in the regulation of CHOP and AS gene transcription in response to amino acid starvation have been partly identified. Particularly, a signalling pathway requiring the protein kinase GCN2 and the transcription factor ATF4 has been described to sense the amino acid limitation. In case of an amino acid imbalanced food source, this pathway has been shown to decrease food intake by activating a neuronal circuit. Taken together, the results discussed in this review demonstrate that amino acids by themselves can act as “signal” molecules with important roles in the control of gene expression and physiological functions.Bien que l'étude du rôle des nutriments dans la régulation de l'expression des gènes chez les Mammifères soit devenue un domaine de recherche important les mécanismes impliquant les acides aminés sont encore peu connus. Du fait de l'importance de leurs rôles physiologiques, l'homéostasie des acides aminés doit être finement régulée. Cependant, les concentrations plasmatiques des acides aminés peuvent être affectées par certaines conditions nutritionnelles ou différentes formes d'agression. En régulant l'expression d'un grand nombre de gènes, l'organisme a la capacité d'ajuster certaines de ses fonctions impliquées dans l'adaptation à la disponibilité en acides aminés. Cette revue vise à rassembler les données actuelles concernant le rôle des acides aminés dans la régulation de l'expression des gènes et des fonctions physiologiques chez les Mammifères. Pour plusieurs acides aminés dits « indispensables », une diminution de leur concentration entraîne la stimulation de l'expression de gènes cibles spécifiques tels que les gènes codant pour IGFBP-1, CHOP et l'asparagine synthétase (AS). Les mécanismes moléculaires impliqués dans l'activation transcriptionnelle de CHOP et AS en réponse à une carence en acide aminé ont été en partie identifiés. En particulier, une voie de signalisation faisant intervenir la protéine kinase GCN2 et le facteur de transcription ATF4 joue le rôle de senseur des déficits en acides aminés. Au niveau physiologique, des travaux récents montrent que l'activation de cette voie permet par le biais d'un circuit neuronal, d'inhiber la prise alimentaire lorsque l'apport nutritionnel en acides aminés est déséquilibré. L'ensemble des données présentées dans cette revue montre que les acides aminés peuvent agir comme des molécules « signal » contrôlant l'expression de gènes afin de réguler certaines fonctions physiologiques

Nucleus accumbens controls wakefulness by a subpopulation of neurons expressing dopamine D1 receptors

Nucleus accumbens (NAc) is involved in behaviors that depend on heightened wakefulness, but its impact on arousal remains unclear. Here, we demonstrate that NAc dopamine D1 receptor (D1R)-expressing neurons are essential for behavioral arousal. Using in vivo fiber photometry in mice, we find arousal-dependent increases in population activity of NAc D1R neurons. Optogenetic activation of NAc D1R neurons induces immediate transitions from non-rapid eye movement sleep to wakefulness, and chemogenetic stimulation prolongs arousal, with decreased food intake. Patch-clamp, tracing, immunohistochemistry, and electron microscopy reveal that NAc D1R neurons project to the midbrain and lateral hypothalamus, and might disinhibit midbrain dopamine neurons and lateral hypothalamus orexin neurons. Photoactivation of terminals in the midbrain and lateral hypothalamus is sufficient to induce wakefulness. Silencing of NAc D1R neurons suppresses arousal, with increased nest-building behaviors. Collectively, our data indicate that NAc D1R neuron circuits are essential for the induction and maintenance of wakefulness

The Leptomeninges Produce Prostaglandin D2 Involved in Sleep Regulation in Mice

Injection of nanomolar amounts of prostaglandin D2 (PGD2) into the rat brain has dose and time-dependent somnogenic effects, and the PGD2-induced sleep is indistinguishable from physiologic sleep. Sleep-inducing PGD2 is produced in the brain by lipocalin-type PGD2 synthase (LPGDS). Three potential intracranial sources of LPGDS have been identified: oligodendrocytes, choroid plexus, and leptomeninges. We aimed at the identification of the site of synthesis of somnogenic PGD2 and therefore, generated a transgenic mouse line with the LPGDS gene amenable to conditional deletion using Cre recombinase (flox-LPGDS mouse). To identify the cell type responsible for producing somnogenic PGD2, we engineered animals lacking LPGDS expression specifically in oligodendrocytes (OD-LPGDS KO), choroid plexus (CP-LPGDS KO), or leptomeninges (LM-LPGDS KO). We measured prostaglandins and LPGDS concentrations together with PGD synthase activity in the brain of these mice. While the LPGDS amount and PGD synthase activity were drastically reduced in the OD- and LM-LPGDS KO mice, they were unchanged in the CP-LPGDS KO mice compared with control animals. We then recorded electroencephalograms, electromyograms, and locomotor activity to measure sleep in 10-week-old mice with specific knockdown of LPGDS in each of the three targets. Using selenium tetrachloride, a specific PGDS inhibitor, we demonstrated that sleep is inhibited in OD-LPGDS and CP-LPGDS KO mice, but not in the LM-LPGDS KO mice. We concluded that somnogenic PGD2 is produced primarily by the leptomeninges, and not by oligodendrocytes or choroid plexus

Combining two-photon photoemission and transient absorption spectroscopy to resolve hot carrier cooling in 2D perovskite single crystals: the effect of surface layer

We investigate hot carrier (HC) cooling in two-dimensional (2D) perovskite single crystals by applying two complementary ultrafast spectroscopy techniques – transient absorption (TA) and time-resolved two-photon photoemission (TR-2PPE) spectroscopies. TR-2PPE directly maps the hot electron distribution and its dynamics in the conduction band to the detected photoelectron distribution. While TR-2PPE selectively probes the upper layer of the material, TA provides information on the whole bulk. Two cooling regimes are resolved in both techniques. The fast timescale of 100–200 fs is related to the electron scattering by longitudinal optical (LO) phonons and the slow timescale of 3–4 ps corresponds to the LO phonon relaxation. The HC cooling dynamic of TA measurement has faster initial stage and higher starting temperature for the slower stage than in TR-2PPE measurements. Conclusions about spatial sensitivity of the cooling dynamics across the 2D perovskite single crystals constitute valuable information that can guide the future development of HC solar cells and thermoelectric applications based on 2D perovskites

Striatal adenosine A2A receptor neurons control active-period sleep via parvalbumin neurons in external globus pallidus

Dysfunction of the striatum is frequently associated with sleep disturbances. However, its role in sleep-wake regulation has been paid little attention even though the striatum densely expresses adenosine A2A receptors (A2ARs), which are essential for adenosine-induced sleep. Here we showed that chemogenetic activation of A2AR neurons in specific subregions of the striatum induced a remarkable increase in non-rapid eye movement (NREM) sleep. Anatomical mapping and immunoelectron microscopy revealed that striatal A2AR neurons innervated the external globus pallidus (GPe) in a topographically organized manner and preferentially formed inhibitory synapses with GPe parvalbumin (PV) neurons. Moreover, lesions of GPe PV neurons abolished the sleep-promoting effect of striatal A2AR neurons. In addition, chemogenetic inhibition of striatal A2AR neurons led to a significant decrease of NREM sleep at active period, but not inactive period of mice. These findings reveal a prominent contribution of striatal A2AR neuron/GPe PV neuron circuit in sleep control

Slow-wave sleep is controlled by a subset of nucleus accumbens core neurons in mice

Sleep control is ascribed to a two-process model, a widely accepted concept that posits homoeostatic drive and a circadian process as the major sleep-regulating factors. Cognitive and emotional factors also influence sleep–wake behaviour; however, the precise circuit mechanisms underlying their effects on sleep control are unknown. Previous studies suggest that adenosine has a role affecting behavioural arousal in the nucleus accumbens (NAc), a brain area critical for reinforcement and reward. Here, we show that chemogenetic or optogenetic activation of excitatory adenosine A2A receptor-expressing indirect pathway neurons in the core region of the NAc strongly induces slow-wave sleep. Chemogenetic inhibition of the NAc indirect pathway neurons prevents the sleep induction, but does not affect the homoeostatic sleep rebound. In addition, motivational stimuli inhibit the activity of ventral pallidum-projecting NAc indirect pathway neurons and suppress sleep. Our findings reveal a prominent contribution of this indirect pathway to sleep control associated with motivation