Ongoing accumulation of plant diversity through habitat connectivity in an 18-year experiment.

Deleterious effects of habitat fragmentation and benefits of connecting fragments could be significantly underestimated because changes in colonization and extinction rates that drive changes in biodiversity can take decades to accrue. In a large and well-replicated habitat fragmentation experiment, we find that annual colonization rates for 239 plant species in connected fragments are 5% higher and annual extinction rates 2% lower than in unconnected fragments. This has resulted in a steady, nonasymptotic increase in diversity, with nearly 14% more species in connected fragments after almost two decades. Our results show that the full biodiversity value of connectivity is much greater than previously estimated, cannot be effectively evaluated at short time scales, and can be maximized by connecting habitat sooner rather than later.

Effects of explicit atmospheric convection at high CO2.

The effect of clouds on climate remains the largest uncertainty in climate change predictions, due to the inability of global climate models (GCMs) to resolve essential small-scale cloud and convection processes. We compare preindustrial and quadrupled CO2 simulations between a conventional GCM in which convection is parameterized and a "superparameterized" model in which convection is explicitly simulated with a cloud-permitting model in each grid cell. We find that the global responses of the two models to increased CO2 are broadly similar: both simulate ice-free Arctic summers, wintertime Arctic convection, and enhanced Madden-Julian oscillation (MJO) activity. Superparameterization produces significant differences at both CO2 levels, including greater Arctic cloud cover, further reduced sea ice area at high CO2, and a stronger increase with CO2 of the MJO.

Prenatal immune activation interacts with stress and corticosterone exposure later in life to modulate N-methyl-D-aspartate receptor synaptic function and plasticity.

Prenatal infection is an environmental risk factor for schizophrenia while later in life, stressful events have been associated with the onset and severity of psychosis. Recent findings on the impact of stress on the N-methyl-d-aspartate receptor (NMDAR), of which hypofunctioning is implicated in schizophrenia, suggest changes in stress-induced regulation of the glutamatergic system may be related to the pathogenesis of schizophrenia. Our study aimed to test whether prenatal immune activation could interact with stress at adolescence to alter NMDAR function. We used offspring from rat dams administered bacterial lipopolysaccharide (LPS) during pregnancy (gestational days 15 and 16), an animal model expressing schizophrenia-related behavioural phenotypes. Using electrophysiological techniques, we investigated effects of stress and the stress hormone corticosterone (Cort) on NMDAR-mediated synaptic function and long-term depression (LTD) in hippocampal CA1 slices from these adolescent (aged 28-39 d) male offspring. In prenatal LPS offspring, NMDAR-mediated synaptic function and LTD were reduced and abolished, respectively, compared to prenatal saline controls. Notably, in vivo stress and in vitro Cort treatment facilitated LTD in slices from prenatal LPS rats but not prenatal saline controls. Finally, Cort enhanced NMDAR-mediated synaptic function in slices from prenatal LPS rats only. We conclude that prenatal immune activation results in NMDAR hypofunction in the hippocampus of adolescent rats but also increases responsiveness of NMDAR-mediated synaptic function and LTD towards stress. Prenatal infection could confer susceptibility to schizophrenia through modification of hippocampal NMDAR function, with hypofunction in resting conditions and heightened responsiveness to stress, thus impacting the development of the disorder.

Altered responses to novelty and drug reinforcement in adult rats treated neonatally with domoic acid.

Activity in the mesocorticolimbic dopamine system is linked to responses to novelty, reward, and drug-seeking behaviours. Glutamate signaling, through kainate receptors, has been shown to modulate dopamine release in this pathway. In the present study, a low, overtly non-convulsive dose of the kainate receptor agonist, domoic acid (DOM), was administered to rat pups over PND 8-14. As juveniles and adolescents, rats were assessed in the open field. During adulthood, rats were tested in an open field, a sucrose consumption task, the playground maze and in a nicotine-induced conditioned place preference paradigm. Domoic acid related effects were found in open field behavior at each time point assessed. Male rats treated neonatally with DOM displayed altered novelty-related behaviour in a novelty trial, as indicated by an increase in time spent exploring familiar objects during the novelty trial of the playground maze. In nicotine-induced conditioned place preference, DOM-treated females developed a conditioned place preference for the nicotine-paired compartment of the test arena, an effect that was maintained for at least a month following the final drug-compartment pairing. The results of this study underscore the importance of the glutamate system in the ontogeny of behaviors that rely on the functional integrity of the midbrain dopamine system.