Concentrations and fluxes of isoprene and oxygenated VOCs at a French Mediterranean oak forest

The CANOPEE project aims to better understand the biosphere–atmosphere exchanges of biogenic volatile organic compounds (BVOCs) in the case of Mediterranean ecosystems and the impact of in-canopy processes on the atmospheric chemical composition above the canopy. Based on an intensive field campaign, the objective of our work was to determine the chemical composition of the air inside a canopy as well as the net fluxes of reactive species between the canopy and the boundary layer. Measurements were carried out during spring 2012 at the field site of the Oak Observatory of the Observatoire de Haute Provence (O3HP) located in the southeast of France. The site is a forest ecosystem dominated by downy oak, Quercus pubescens Willd., a typical Mediterranean species which features large isoprene emission rates. Mixing ratios of isoprene, its degradation products methylvinylketone (MVK) and methacrolein (MACR) and several other oxygenated VOC (OxVOC) were measured above the canopy using an online proton transfer reaction mass spectrometer (PTR-MS), and fluxes were calculated by the disjunct eddy covariance approach. The O3HP site was found to be a very significant source of isoprene emissions, with daily maximum ambient concentrations ranging between 2–16 ppbv inside and 2–5 ppbv just above the top of the forest canopy. Significant isoprene fluxes were observed only during daytime, following diurnal cycles with midday net emission fluxes from the canopy ranging between 2.0 and 9.7 mg m−2 h1. Net isoprene normalized flux (at 30 °C, 1000 μmol quanta m−2 s−1) was estimated at 7.4 mg m−2 h−1. Evidence of direct emission of methanol was also found exhibiting maximum daytime fluxes ranging between 0.2 and 0.6 mg m−2 h−1, whereas flux values for monoterpenes and others OxVOC such as acetone and acetaldehyde were below the detection limit. The MVK+MACR-to-isoprene ratio provided useful information on the oxidation of isoprene, and is in agreement with recent findings proposing weak production yields of MVK and MACR, in remote forest regions where the NOx concentrations are low. In-canopy chemical oxidation of isoprene was found to be weak and did not seem to have a significant impact on isoprene concentrations and fluxes above the canopy

Brainstem and Spinal Cord Circuitry Regulating REM Sleep and Muscle Atonia

Previous work has suggested, but not demonstrated directly, a critical role for both glutamatergic and GABAergic neurons of the pontine tegmentum in the regulation of rapid eye movement (REM) sleep.To determine the in vivo roles of these fast-acting neurotransmitters in putative REM pontine circuits, we injected an adeno-associated viral vector expressing Cre recombinase (AAV-Cre) into mice harboring lox-P modified alleles of either the vesicular glutamate transporter 2 (VGLUT2) or vesicular GABA-glycine transporter (VGAT) genes. Our results show that glutamatergic neurons of the sublaterodorsal nucleus (SLD) and glycinergic/GABAergic interneurons of the spinal ventral horn contribute to REM atonia, whereas a separate population of glutamatergic neurons in the caudal laterodorsal tegmental nucleus (cLDT) and SLD are important for REM sleep generation. Our results further suggest that presynaptic GABA release in the cLDT-SLD, ventrolateral periaqueductal gray matter (vlPAG) and lateral pontine tegmentum (LPT) are not critically involved in REM sleep control.These findings reveal the critical and divergent in vivo role of pontine glutamate and spinal cord GABA/glycine in the regulation of REM sleep and atonia and suggest a possible etiological basis for REM sleep behavior disorder (RBD)

Morphological investigation of polylactide/microfibrillated cellulose composites

Optical microscopy and transmission electron microscopy have been used to investigate the morphology of polylactide (PLA)/microfibrillated cellulose (MFC) composites prepared by: compression molding of wet-comingled MFC and PLA latex or powder, twin-screw extrusion of the wet-comingled compounds, and solvent mixing of PLA with MFC or acetylated MFC. Compression molding of wet-comingled MFC and PLA latex or powder compounds resulted in a cellular MFC network, whereas solvent-cast films showed a more uniform dispersion of MFC fibers. Somewhat lower aggregate diameters observed in the acetylated MFC were assumed to be due to decreased MFC hydrophilicity and improved chemical affinity with the PLA matrix. The MFC networks in the commingled compounds were severely disrupted after twin-screw extrusion. This confirmed the limited deformability of the networks inferred from the extensive syneresis during the initial compression molding step, and accounted for substantial losses in stiffness reinforcement by the MFC after extrusion

Cholinergic Modulation of Narcoleptic Attacks in Double Orexin Receptor Knockout Mice

To investigate how cholinergic systems regulate aspects of the sleep disorder narcolepsy, we video-monitored mice lacking both orexin (hypocretin) receptors (double knockout; DKO mice) while pharmacologically altering cholinergic transmission. Spontaneous behavioral arrests in DKO mice were highly similar to those reported in orexin-deficient mice and were never observed in wild-type (WT) mice. A survival analysis revealed that arrest lifetimes were exponentially distributed indicating that random, Markovian processes determine arrest lifetime. Low doses (0.01, 0.03 mg/kg, IP), but not a high dose (0.08 mg/kg, IP) of the cholinesterase inhibitor physostigmine increased the number of arrests but did not alter arrest lifetimes. The muscarinic antagonist atropine (0.5 mg/kg, IP) decreased the number of arrests, also without altering arrest lifetimes. To determine if muscarinic transmission in pontine areas linked to REM sleep control also influences behavioral arrests, we microinjected neostigmine (50 nl, 62.5 µM) or neostigmine + atropine (62.5 µM and 111 µM respectively) into the nucleus pontis oralis and caudalis. Neostigmine increased the number of arrests in DKO mice without altering arrest lifetimes but did not provoke arrests in WT mice. Co-injection of atropine abolished this effect. Collectively, our findings establish that behavioral arrests in DKO mice are similar to those in orexin deficient mice and that arrests have exponentially distributed lifetimes. We also show, for the first time in a rodent narcolepsy model, that cholinergic systems can regulate arrest dynamics. Since perturbations of muscarinic transmission altered arrest frequency but not lifetime, our findings suggest cholinergic systems influence arrest initiation without influencing circuits that determine arrest duration

Trail formation based on directed pheromone deposition

We propose an Individual-Based Model of ant-trail formation. The ants are modeled as self-propelled particles which deposit directed pheromones and interact with them through alignment interaction. The directed pheromones intend to model pieces of trails, while the alignment interaction translates the tendency for an ant to follow a trail when it meets it. Thanks to adequate quantitative descriptors of the trail patterns, the existence of a phase transition as the ant-pheromone interaction frequency is increased can be evidenced. Finally, we propose both kinetic and fluid descriptions of this model and analyze the capabilities of the fluid model to develop trail patterns. We observe that the development of patterns by fluid models require extra trail amplification mechanisms that are not needed at the Individual-Based Model level

Role of the Lateral Paragigantocellular Nucleus in the Network of Paradoxical (REM) Sleep: An Electrophysiological and Anatomical Study in the Rat

The lateral paragigantocellular nucleus (LPGi) is located in the ventrolateral medulla and is known as a sympathoexcitatory area involved in the control of blood pressure. In recent experiments, we showed that the LPGi contains a large number of neurons activated during PS hypersomnia following a selective deprivation. Among these neurons, more than two-thirds are GABAergic and more than one fourth send efferent fibers to the wake-active locus coeruleus nucleus. To get more insight into the role of the LPGi in PS regulation, we combined an electrophysiological and anatomical approach in the rat, using extracellular recordings in the head-restrained model and injections of tracers followed by the immunohistochemical detection of Fos in control, PS-deprived and PS-recovery animals. With the head-restrained preparation, we showed that the LPGi contains neurons specifically active during PS (PS-On neurons), neurons inactive during PS (PS-Off neurons) and neurons indifferent to the sleep-waking cycle. After injection of CTb in the facial nucleus, the neurons of which are hyperpolarized during PS, the largest population of Fos/CTb neurons visualized in the medulla in the PS-recovery condition was observed in the LPGi. After injection of CTb in the LPGi itself and PS-recovery, the nucleus containing the highest number of Fos/CTb neurons, moreover bilaterally, was the sublaterodorsal nucleus (SLD). The SLD is known as the pontine executive PS area and triggers PS through glutamatergic neurons. We propose that, during PS, the LPGi is strongly excited by the SLD and hyperpolarizes the motoneurons of the facial nucleus in addition to local and locus coeruleus PS-Off neurons, and by this means contributes to PS genesis

A Very Large Number of GABAergic Neurons Are Activated in the Tuberal Hypothalamus during Paradoxical (REM) Sleep Hypersomnia

We recently discovered, using Fos immunostaining, that the tuberal and mammillary hypothalamus contain a massive population of neurons specifically activated during paradoxical sleep (PS) hypersomnia. We further showed that some of the activated neurons of the tuberal hypothalamus express the melanin concentrating hormone (MCH) neuropeptide and that icv injection of MCH induces a strong increase in PS quantity. However, the chemical nature of the majority of the neurons activated during PS had not been characterized. To determine whether these neurons are GABAergic, we combined in situ hybridization of GAD67 mRNA with immunohistochemical detection of Fos in control, PS deprived and PS hypersomniac rats. We found that 74% of the very large population of Fos-labeled neurons located in the tuberal hypothalamus after PS hypersomnia were GAD-positive. We further demonstrated combining MCH immunohistochemistry and GAD67 in situ hybridization that 85% of the MCH neurons were also GAD-positive. Finally, based on the number of Fos-ir/GAD+, Fos-ir/MCH+, and GAD+/MCH+ double-labeled neurons counted from three sets of double-staining, we uncovered that around 80% of the large number of the Fos-ir/GAD+ neurons located in the tuberal hypothalamus after PS hypersomnia do not contain MCH. Based on these and previous results, we propose that the non-MCH Fos/GABAergic neuronal population could be involved in PS induction and maintenance while the Fos/MCH/GABAergic neurons could be involved in the homeostatic regulation of PS. Further investigations will be needed to corroborate this original hypothesis

Circuit-based interrogation of sleep control.

Sleep is a fundamental biological process observed widely in the animal kingdom, but the neural circuits generating sleep remain poorly understood. Understanding the brain mechanisms controlling sleep requires the identification of key neurons in the control circuits and mapping of their synaptic connections. Technical innovations over the past decade have greatly facilitated dissection of the sleep circuits. This has set the stage for understanding how a variety of environmental and physiological factors influence sleep. The ability to initiate and terminate sleep on command will also help us to elucidate its functions within and beyond the brain

Recent decreases in fossil-fuel emissions of ethane and methane derived from firn air

Methane and ethane are the most abundant hydrocarbons in the atmosphere and they affect both atmospheric chemistry and climate. Both gases are emitted from fossil fuels and biomass burning, whereas methane (CH(4)) alone has large sources from wetlands, agriculture, landfills and waste water. Here we use measurements in firn (perennial snowpack) air from Greenland and Antarctica to reconstruct the atmospheric variability of ethane (C(2)H(6)) during the twentieth century. Ethane levels rose from early in the century until the 1980s, when the trend reversed, with a period of decline over the next 20 years. We find that this variability was primarily driven by changes in ethane emissions from fossil fuels; these emissions peaked in the 1960s and 1970s at 14-16 teragrams per year (1 Tg = 10(12) g) and dropped to 8-10 Tg  yr(-1) by the turn of the century. The reduction in fossil-fuel sources is probably related to changes in light hydrocarbon emissions associated with petroleum production and use. The ethane-based fossil-fuel emission history is strikingly different from bottom-up estimates of methane emissions from fossil-fuel use, and implies that the fossil-fuel source of methane started to decline in the 1980s and probably caused the late twentieth century slow-down in the growth rate of atmospheric methane