Chromium stable isotope distributions in the southwest Pacific Ocean and constraints on hydrothermal input from the Kermadec Arc

Special attention has been given to chromium (Cr) as a paleoproxy tracing redox cycling throughout Earth’s history, due to differences in the solubility of its primary redox species at Earth’s surface (Cr (III) and Cr(VI)) and isotope fractionation associated with their interconversion. In turn, chromium’s pale- oproxy potential has motivated studies of the modern ocean to better understand which processes drive its cycling and to constrain their impact on the Cr isotope composition (d53Cr) of seawater. Here, we pre- sent total dissolved seawater Cr concentrations and d53Cr along the GEOTRACES GP13 section. This sec- tion is a zonal transect extending from Australia in the subtropical southwest Pacific Ocean. Surface signals of local biological Cr cycling are minimal, in agreement with distributions of dissolved major nutrients as well as biologically-controlled trace metals in this low productivity, oligotrophic environ- ment. Depth profiles have Cr concentration minima in surface waters and maxima at depth, and are lar- gely shaped by the advection of nutrient- and Cr-rich subsurface waters rather than vertically-driven processes. Samples close to the sediment–water interface indicate important benthic Cr fluxes across the section. The GP13 transect crosses the hydrothermally-active Kermadec Arc. Hydrothermal fluids (consisting of <15% background seawater) were collected from three venting sites at the Brothers Volcano (along the Kermadec Arc). These fluids yielded near-crustal d53Cr values (!0.17 to +0.08‰) and elevated [Cr] (7.5–23 nmol kg!1, hydrothermal endmember [Cr] % 8–27 nmol kg!1), indicating that the Kermadec Arc may be an isotopically light Cr source. Dissolved [Fe] enrichments have been reported previously in deep waters ($1600–3000 m) along the GP13 transect, east of the Kermadec Arc. These same waters show ele- vated [Cr] compared to Circumpolar Deep Water ([Cr] = 3.88 ± 0.11, d53Cr = 0.89 ± 0.08, n = 32), with an aver- age [Cr] accumulation of 0.71 ± 0.11 nmol kg!1 (1 SD), and an estimated d53Cr of +0.46 ± 0.30‰ (2 SD, n = 9) for the accumulated Cr. Comparing high-temperature vent and neutrally buoyant plume data, hydrothermal-sourced Cr is likely negligable compared to Cr contributions from other processes (benthic fluxes, release from particles), and the advection of more Cr-rich Pacific Deep Water. It is unlikely that hydrothermal vents would be a major contributor within the regional or global biogeochemical Cr cycle, even if hydrothermal fluxes change by orders of magnitude, and therefore d53Cr trends in the paleorecord may be attributable, at least in part, to major changes in other controls on Cr (e.g. widespread anoxia)

Upregulation of the voltage-gated sodium channel beta2 subunit in neuropathic pain models: characterization of expression in injured and non-injured primary sensory neurons

The development of abnormal primary sensory neuron excitability and neuropathic pain symptoms after peripheral nerve injury is associated with altered expression of voltage-gated sodium channels (VGSCs) and a modification of sodium currents. To investigate whether the beta2 subunit of VGSCs participates in the generation of neuropathic pain, we used the spared nerve injury (SNI) model in rats to examine beta2 subunit expression in selectively injured (tibial and common peroneal nerves) and uninjured (sural nerve) afferents. Three days after SNI, immunohistochemistry and Western blot analysis reveal an increase in the beta2 subunit in both the cell body and peripheral axons of injured neurons. The increase persists for >4 weeks, although beta2 subunit mRNA measured by real-time reverse transcription-PCR and in situ hybridization remains unchanged. Although injured neurons show the most marked upregulation,beta2 subunit expression is also increased in neighboring non-injured neurons and a similar pattern of changes appears in the spinal nerve ligation model of neuropathic pain. That increased beta2 subunit expression in sensory neurons after nerve injury is functionally significant, as demonstrated by our finding that the development of mechanical allodynia-like behavior in the SNI model is attenuated in beta2 subunit null mutant mice. Through its role in regulating the density of mature VGSC complexes in the plasma membrane and modulating channel gating, the beta2 subunit may play a key role in the development of ectopic activity in injured and non-injured sensory afferents and, thereby, neuropathic pain

Raptor-Mediated Proteasomal Degradation of Deamidated 4E-BP2 Regulates Postnatal Neuronal Translation and NF-κB Activity

The translation initiation repressor 4E-BP2 is deamidated in the brain on asparagines N99/N102 during early postnatal brain development. This post-translational modification enhances 4E-BP2 association with Raptor, a central component of mTORC1 and alters the kinetics of excitatory synaptic transmission. We show that 4E-BP2 deamidation is neuron specific, occurs in the human brain, and changes 4E-BP2 subcellular localization, but not its disordered structure state. We demonstrate that deamidated 4E-BP2 is ubiquitinated more and degrades faster than the unmodified protein. We find that enhanced deamidated 4E-BP2 degradation is dependent on Raptor binding, concomitant with increased association with a Raptor-CUL4B E3 ubiquitin ligase complex. Deamidated 4E-BP2 stability is promoted by inhibiting mTORC1 or glutamate receptors. We further demonstrate that deamidated 4E-BP2 regulates the translation of a distinct pool of mRNAs linked to cerebral development, mitochondria, and NF-κB activity, and thus may be crucial for postnatal brain development in neurodevelopmental disorders, such as ASD

Enduring neurobehavioral effects induced by microbiota depletion during the adolescent period

The gut microbiota is an essential regulator of many aspects of host physiology. Disruption of gut microbial communities affects gut-brain communication which ultimately can manifest as changes in brain function and behaviour. Transient changes in gut microbial composition can be induced by various intrinsic and extrinsic factors, however, it is possible that enduring shifts in the microbiota composition can be achieved by perturbation at a timepoint when the gut microbiota has not fully matured or is generally unstable, such as during early life or ageing. In this study, we investigated the effects of 3-week microbiota depletion with antibiotic treatment during the adolescent period and in adulthood. Following a washout period to restore the gut microbiota, behavioural and molecular hallmarks of gut-brain communication were investigated. Our data revealed that transient microbiota depletion had long-lasting effects on microbiota composition and increased anxiety-like behaviour in mice exposed to antibiotic treatment during adolescence but not in adulthood. Similarly, gene expression in the amygdala was more severely affected in mice treated during adolescence. Taken together these data highlight the vulnerability of the gut microbiota during the critical adolescent period and the long-lasting impact manipulations of the microbiota can have on gene expression and behaviour in adulthood

Enduring neurobehavioral effects induced by microbiota depletion during the adolescent period

Peer ReviewedThe gut microbiota is an essential regulator of many aspects of host physiology. Disruption of gut microbial communities affects gut-brain communication which ultimately can manifest as changes in brain function and behaviour. Transient changes in gut microbial composition can be induced by various intrinsic and extrinsic factors, however, it is possible that enduring shifts in the microbiota composition can be achieved by perturbation at a timepoint when the gut microbiota has not fully matured or is generally unstable, such as during early life or ageing. In this study, we investigated the effects of 3-week microbiota depletion with antibiotic treatment during the adolescent period and in adulthood. Following a washout period to restore the gut microbiota, behavioural and molecular hallmarks of gut-brain communication were investigated. Our data revealed that transient microbiota depletion had long-lasting effects on microbiota composition and increased anxiety-like behaviour in mice exposed to antibiotic treatment during adolescence but not in adulthood. Similarly, gene expression in the amygdala was more severely affected in mice treated during adolescence. Taken together these data highlight the vulnerability of the gut microbiota during the critical adolescent period and the long-lasting impact manipulations of the microbiota can have on gene expression and behaviour in adulthood.Science Foundation Irelan

18 years of the European Journal of Wildlife Research: profile and prospects

Expanding on the foundation of Zeitschrift für Jagdwissenschaft in 1955, the European Journal of Wildlife Research (EJWR) continues to publish original research and reviews on all aspects of wildlife science regardless of the geographic region. Eighteen years after publication of the first issue of EJWR, we briefly reflect on the journal’s profile and prospects. Our target audience includes researchers, wildlife biologists, forestry and game management professionals, wildlife veterinarians, and other specialists, but we also aim at providing a resource of relevant information and scientific debate for practitioners and every person interested in wildlife science. With ecosystems being at the highest level of pressure due to land use change and other effects of the global crisis, the journal is in a key position to communicate relevant research to the scientific community around the world.Peer reviewe

Uncovering memory-related gene expression in contextual fear conditioning using ribosome profiling

Contextual fear conditioning (CFC) in rodents is the most widely used behavioural paradigm in neuroscience research to elucidate the neurobiological mechanisms underlying learning and memory. It is based on the pairing of an aversive unconditioned stimulus (US; e.g. mild footshock) with a neutral conditioned stimulus (CS; e.g. context of the test chamber) in order to acquire associative long-term memory (LTM), which persists for days and even months. Using genome-wide analysis, several studies have generated lists of genes modulated in response to CFC in an attempt to identify the "memory genes", which orchestrate memory formation. Yet, most studies use naïve animals as a baseline for assessing gene-expression changes, while only few studies have examined the effect of the US alone, without pairing to context, using genome-wide analysis of gene-expression. Herein, using the ribosome profiling methodology, we show that in male mice an immediate shock, which does not lead to LTM formation, elicits pervasive translational and transcriptional changes in the expression of Immediate Early Genes (IEGs) in dorsal hippocampus (such as Fos and Arc), a fact which has been disregarded by the majority of CFC studies. By removing the effect of the immediate shock, we identify and validate a new set of genes, which are translationally and transcriptionally responsive to the association of context-to-footshock in CFC, and thus constitute salient "memory genes"

Ultrastructural changes of the intracellular surfactant pool in a rat model of lung transplantation-related events

<p>Abstract</p> <p>Background</p> <p>Ischemia/reperfusion (I/R) injury, involved in primary graft dysfunction following lung transplantation, leads to inactivation of intra-alveolar surfactant which facilitates injury of the blood-air barrier. The alveolar epithelial type II cells (AE2 cells) synthesize, store and secrete surfactant; thus, an intracellular surfactant pool stored in lamellar bodies (Lb) can be distinguished from the intra-alveolar surfactant pool. The aim of this study was to investigate ultrastructural alterations of the intracellular surfactant pool in a model, mimicking transplantation-related procedures including flush perfusion, cold ischemia and reperfusion combined with mechanical ventilation.</p> <p>Methods</p> <p>Using design-based stereology at the light and electron microscopic level, number, surface area and mean volume of AE2 cells as well as number, size and total volume of Lb were determined in a group subjected to transplantation-related procedures including both I/R injury and mechanical ventilation (I/R group) and a control group.</p> <p>Results</p> <p>After I/R injury, the mean number of Lb per AE2 cell was significantly reduced compared to the control group, accompanied by a significant increase in the luminal surface area per AE2 cell in the I/R group. This increase in the luminal surface area correlated with the decrease in surface area of Lb per AE2. The number-weighted mean volume of Lb in the I/R group showed a tendency to increase.</p> <p>Conclusion</p> <p>We suggest that in this animal model the reduction of the number of Lb per AE2 cell is most likely due to stimulated exocytosis of Lb into the alveolar space. The loss of Lb is partly compensated by an increased size of Lb thus maintaining total volume of Lb per AE2 cell and lung. This mechanism counteracts at least in part the inactivation of the intra-alveolar surfactant.</p