The N2-fixing shrub Amorpha fruticosa L. is rapidly spreading in the dry riparian natural grasslands of Europe, altering ecosystem functions and depleting plant diversity. Alteration of the N cycle ...represents the key factor involved in invasions by N2-fixing plants with cascading effects on plant species richness. We hypothesized that A. fruticosa encroachment strongly impacts not only the N but also the C cycle and that the magnitude of such alterations may be modulated by soil characteristics. To test these hypotheses, we selected four river floodplains in North East of Italy and compared natural uninvaded grasslands with half invaded and completely invaded sites, based on A. fruticosa stand characteristic and relevant leaf traits and on soil properties related to soil texture and to C and N cycles. Soil organic matter mineralisation, ammonification and nitrification rates were determined. Soil nitrification increased remarkably with plant invasion while ammonification was significantly higher only in half invaded sites. Soil organic matter mineralisation, microbial biomass C sustained per soil organic C unit and nitrification positively correlated with stand age, regardless to the stage of the encroachment. Mineralisation and nitrification increased with soil organic C and total N in uninvaded and completely invaded sites, but decreased in half invaded sites. At the half invasion stage, trends in nitrification and CO2 mineralisation were transitionally reverted and remediation may be facilitated by less pronounced changes in soil properties compared to completely invaded sites. Direct effects of plant invasion are modulated by the action of soil characteristics such as soil organic C and clay contents, with soils rich in organic C showing larger nitrification and mineralisation rates.
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•Comprehensive study of a vast region undergoing invasion by N2 fixing shrubs•Nitrification increased with SOC at 0% and 100% invasion, but not at 50%.•Direct effects modulated by soil characteristics such as SOC and clay contents.•Plant growth and density affected BC/SOC, but ratios increased with stand age.•Remediation potentially effective at intermediate stage, when trends are reverted.
Epilepsy is one of the most common brain disorder and, despite the possible use of several therapeutic options, many patients continue to have seizures for their entire lifespan and they need new ...therapeutic approaches. In the last years the interest on the non-psychoactive compounds present in Cannabis sativa has massively increased, and cannabidiol (CBD) has been shown to be effective in the treatment of different types of neurological disorders and neurodegenerative diseases such as epilepsy, ischemia, multiple sclerosis and Alzheimer's Disease.
We investigated the effects of the selected cannabinoids, Δ9-tetrahydrocannabinol (THC), CBD and cannabigerol (CBG) in rat organotypic hippocampal slices exposed to kainate, an in vitro seizure model. Cell death in the cornu Ammonis 3 (CA3) hippocampal subregion was quantified by propidium iodide fluorescence. Morphological analysis and tissue organization were examined by immunohistochemistry and confocal microscopy and microglia activation and polarization was evaluated using flow cytometry and morphology analysis.
When present in the incubation medium, cannabidiol reduced dose-dependent CA3 injury induced by kainate. Conversely, incubation with THC exacerbated hippocampal damage. The neuroprotective effects of cannabidiol were blocked by TRPV1, TRPV2, 5-HT1A, and PPARγ antagonists. Confocal microscopy confirmed that CBD but not THC had a significant protective effect against neuronal damage and tissue disorganization caused by kainate. Cannabidiol incubation significantly block the microglia activation from the M0 to M1 phenotype observed in the kainate in-vitro seizure model, pushing toward a transition from M0 to M2.
Our results suggest that CBD mitigated neuronal damage induced by kainate and blocked the transition from the M0 to the M1 phenotype.
•CBD but not THC is neuroprotective in an in-vitro seizure model.•TRPV2 and 5-HT1A receptors mediate the neuroprotective effects of CBD.•CBD but not THC reverts kainate induced microglia phagocytosis of damage neurons.•CBD blocks the transition from an M0 to M1 microglia phenotype induced by kainate.
Modifications in the subunit composition of AMPA receptors (AMPARs) have been linked to the transition from physiological to pathological conditions in a number of contexts, including EtOH‐induced ...neurotoxicity. Previous work from our laboratory showed that EtOH withdrawal causes CA1 pyramidal cell death in organotypic hippocampal slices and changes in the expression of AMPARs. Here, we investigated whether changes in expression and function of AMPARs may be causal for EtOH‐induced neurotoxicity. To this aim, we examined the subunit composition, localization and function of AMPARs in hippocampal slices exposed to EtOH by using western blotting, surface expression assay, confocal microscopy and electrophysiology. We found that EtOH withdrawal specifically increases GluA1 protein signal in total homogenates, but not in the post‐synaptic density‐enriched fraction. This is suggestive of overall increase and redistribution of AMPARs to the extrasynaptic compartment. At functional level, AMPA‐induced calcium influx was unexpectedly reduced, whereas AMPA‐induced current was enhanced in CA1 pyramidal neurons following EtOH withdrawal, suggesting that increased AMPAR expression may lead to cell death because of elevated excitability, and not for a direct contribution on calcium influx. Finally, the neurotoxicity caused by EtOH withdrawal was attenuated by the non‐selective AMPAR antagonist 2,3‐dioxo‐6‐nitro‐1,2,3,4‐tetrahydrobenzofquinoxaline‐7‐sulfonamide disodium salt as well as by the selective antagonist of GluA2‐lacking AMPARs 1‐naphthyl acetyl spermine. We conclude that EtOH neurotoxicity involves changes in expression, surface localization and functional properties of AMPARs, and propose GluA2‐lacking AMPARs as amenable specific targets for the development of neuroprotective drugs in EtOH‐withdrawal syndrome.
Ethanol (EtOH) abuse causes persistent structural and functional alterations in the brain by mechanisms that are not yet fully understood. We studied the changes in molecular composition, protein trafficking and functional properties of glutamate AMPA receptors accompanying ethanol neurotoxicity in rat hippocampal cultures. Our results suggest that EtOH induces profound changes in overall expression, trafficking and molecular composition of AMPA receptors, promoting the expression of a specific subtype of receptors with enhanced function. Subtype‐selective blockers prevent the neurotoxicity induced by EtOH withdrawal, indicating that AMPA receptor subtypes, specifically up‐regulated by chronic EtOH, represent amenable targets for the development of effective neuroprotectants in EtOH toxicity.
We investigated the molecular events triggered by NMDA and 3,5‐dihydroxyphenylglycine (DHPG) preconditioning, that lead to neuroprotection against excitotoxic insults (AMPA or oxygen and glucose ...deprivation) in rat organotypic hippocampal slices, with particular attention on glutamate receptors and on cannabinoid system. We firstly evaluated the protein expression of NMDA and AMPA receptor subunits after preconditioning using western blot analysis performed in post‐synaptic densities. We observed that following NMDA, but not DHPG preconditioning, the expression of GluA1 was significantly reduced and this reduction appeared to be associated with the internalization of AMPA receptors. Whole‐cell voltage clamp recordings on CA1 pyramidal neurons of organotypic slices show that 24 hr after exposure to NMDA and DHPG preconditioning, AMPA‐induced currents were significantly reduced. To clarify the mechanisms induced by DHPG preconditioning, we then investigated the involvement of the endocannabinoid system. Exposure of slices to the CB1 antagonist AM251 prevented the development of tolerance to AMPA toxicity induced by DHPG but not NMDA. Accordingly, the MAG‐lipase inhibitor URB602, that increases arachidonoylglycerol (2‐AG) content, but not the FAAH inhibitor URB597, that limits the degradation of anandamide, was also able to induce tolerance versus AMPA and OGD toxicity, suggesting that 2‐AG is responsible for the DHPG‐induced tolerance. In conclusion, preconditioning with NMDA or DHPG promotes differential neuroprotective mechanisms: NMDA by internalization of GluA1‐AMPA receptors, DHPG by producing the endocannabinoid 2‐AG.
Preconditioning represents an innovative therapeutic strategy that might be utilized to prevent and/or limit stroke in humans, but the underlying mechanisms are still unknown. In this study, we examined the molecular events triggered by NMDA and DHPG preconditioning, with particular attention on the interaction between glutamate neurotransmission and the endocannabinoid system in rat organotypic hippocampal slices. Our results show that NMDA and DHPG preconditioning promote differential neuroprotective mechanisms: NMDA by internalization of GluA1‐AMPA receptors, DHPG by increasing 2‐AG content. These findings shed light on the endogenous neuroprotective mechanisms that may be helpful in designing new strategies for the treatment of cerebral ischemia.
Experimental evidence indicates that the activation of ionotropic glutamate receptors plays an important role in neurological disorders' models such as epilepsy, cerebral ischemia and trauma. The ...glutamate receptor agonist kainic acid (KA) induces seizures and excitotoxic cell death in the CA3 region of the hippocampus. Thymoquinone (TQ) is the most important component of the essential oil obtained from black cumin (
L.) seeds. It has many pharmacological actions including antioxidant, anti-inflammatory, and anti-apoptotic effects. TQ was used in an in vitro experimental model of primary cultures where excitotoxicity was induced. Briefly, rat organotypic hippocampal slices were exposed to 5 µM KA for 24 h. Cell death in the CA3 subregions of slices was quantified by measuring propidium iodide fluorescence. The cross-talk between TQ, ER stress and apoptotic pathways was investigated by Western blot. In untreated slices TQ (10 µM) induced a significant increase on the PSD95 levels and it decreased the excitotoxic injury induced by KA. Additionally, TQ was able to ameliorate the KA-induced increase in unfolded proteins GRP78 and GRP94 expression. Finally, TQ was able to partially rescue the reduction of the KA-induced apoptotic pathway activation. Our results suggest that TQ modulates the processes leading to post-kainate neuronal death in the CA3 hippocampal area.
ABSTRACT
We present the warpfield emission predictor, warpfield-emp, which couples the 1D stellar feedback code warpfield with the cloudy H iiregion/PDR code and the polaris radiative transfer code, ...in order to make detailed predictions for the time-dependent line and continuum emission arising from the H ii region and PDR surrounding an evolving star cluster. warpfield-emp accounts for a wide range of physical processes (photoionization, stellar winds, supernovae, radiation pressure, gravity, thermal conduction, radiative cooling, dust extinction etc.) and yet runs quickly enough to allow us to explore broad ranges of different model parameters. We compare the results of an extensive set of models with SITELLE observations of a large sample of H ii regions in NGC 628 and find very good agreement, particularly for the highest signal-to-noise observations. We show that our approach of modelling individual clouds from first principles (instead of in terms of dimensionless quantities such as the ionization parameter) allows us to avoid long-standing degeneracies in the interpretation of H ii region diagnostics and enables us to relate these diagnostics to important physical parameters such as cloud mass or cluster age. Finally, we explore the implications of our models regarding the reliability of simple metallicity diagnostics, the properties of long-lived embedded clusters, and the role played by winds and supernovae in regulating H ii region and PDR line emission.
Context. To compute the star formation rate (SFR) of galaxies from the rest-frame ultraviolet (UV), it is essential to take the obscuration by dust into account. To do so, one of the most popular ...methods consists in combining the UV with the emission from the dust itself in the infrared (IR). Yet, different studies have derived different estimators, showing that no such hybrid estimator is truly universal. Aims. In this paper we aim at understanding and quantifying what physical processes fundamentally drive the variations between different hybrid estimators. In so doing, we aim at deriving new universal UV+IR hybrid estimators to correct the UV for dust attenuation at local and global scales, taking the intrinsic physical properties of galaxies into account. Methods. We use the CIGALE code to model the spatially resolved far-UV to far-IR spectral energy distributions of eight nearby star-forming galaxies drawn from the KINGFISH sample. This allows us to determine their local physical properties, and in particular their UV attenuation, average SFR, average specific SFR (sSFR), and their stellar mass. We then examine how hybrid estimators depend on said properties. Results. We find that hybrid UV+IR estimators strongly depend on the stellar mass surface density (in particular at 70 μm and 100 μm) and on the sSFR (in particular at 24 μm and the total infrared). Consequently, the IR scaling coefficients for UV obscuration can vary by almost an order of magnitude: from 1.55 to 13.45 at 24 μm for instance. This result contrasts with other groups who found relatively constant coefficients with small deviations. We exploit these variations to construct a new class of adaptative hybrid estimators based on observed UV to near-IR colours and near-IR luminosity densities per unit area. We find that they can reliably be extended to entire galaxies. Conclusions. The new estimators provide better estimates of attenuation-corrected UV emission than classical hybrid estimators published in the literature. Taking naturally variable impact of dust heated by old stellar populations into account, they constitute an important step towards universal estimators.
Verticillium dahliae
(Kleb.) is a soil-borne pathogen able to cause yield losses in eggplant,
Solanum melongena
L., one of the most important vegetable crops in the Mediterranean basin. In this ...study, an experiment was conducted to assess physiological and biochemical mechanisms modulating the interactions between
S. melongena
cv. Violetta di Rimini and
V. dahliae
strain VdGL16 in leaves at different age (mature, intermediate and young; ML, IL and YL) up to 25 days post artificial root inoculation (dpi). At 8 dpi, infected ML showed a marked reduction of photosynthetic rate (4-fold lower than controls) associated with stomatal (reduced stomatal conductance) and mesophyll (concomitant increase of intercellular CO
2
concentration) limitations. Cell membrane integrity was compromised, and phylloptosis/death occurred. At 8 and 18 dpi, stomatal closure (−40 and − 53%, respectively) and biochemical alterations occurred in IL. At 18 dpi, the consumption of secondary metabolites suggested that antioxidant- and antimicrobial-defence responses were activated. However, photoinhibition, oxidative stress and water deficit were observed at the end of the experiment. These mechanisms were observed also in YL, as confirmed by the strong increase of tannins (+46%) followed by accumulation of other phenylpropanoids. Despite plant growth being maintained, reduction of leaf area and water deficit occurred. This study highlights the capacity of eggplant to activate dynamic biochemical mechanisms in response to fungal infection, even in susceptible genotypes, a starting point for comparisons with resistant material for selection.
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![Synthetic [C ii] emission m...](http://api.summon.serialssolutions.com/2.0.0/image/issn/XR4PS5YY4K/0035-8711_1365-8711_1365-2966/small "Synthetic [C ii] emission maps of a simulated molecular cloud in formation")
