Evaluation of coupled ocean-atmosphere simulations of northern hemisphere extratropical climates in the mid-Holocene

We have used the BIOME4 biogeography–biochemistry model and comparison with palaeovegetation data to evaluate the response of six ocean–atmosphere general circulation models to mid-Holocene changes in orbital forcing in the mid- to high-latitudes of the northern hemisphere. All the models produce: (a) a northward shift of the northern limit of boreal forest, in response to simulated summer warming in high-latitudes. The northward shift is markedly asymmetric, with larger shifts in Eurasia than in North America; (b) an expansion of xerophytic vegetation in mid-continental North America and Eurasia, in response to increased temperatures during the growing season; (c) a northward expansion of temperate forests in eastern North America, in response to simulated winter warming. The northward shift of the northern limit of boreal forest and the northward expansion of temperate forests in North America are supported by palaeovegetation data. The expansion of xerophytic vegetation in mid-continental North America is consistent with palaeodata, although the extent may be over-estimated. The simulated expansion of xerophytic vegetation in Eurasia is not supported by the data. Analysis of an asynchronous coupling of one model to an equilibrium-vegetation model suggests vegetation feedback exacerbates this mid-continental drying and produces conditions more unlike the observations. Not all features of the simulations are robust: some models produce winter warming over Europe while others produce winter cooling. As a result, some models show a northward shift of temperate forests (consistent with, though less marked than, the expansion shown by data) and others produce a reduction in temperate forests. Elucidation of the cause of such differences is a focus of the current phase of the Palaeoclimate Modelling Intercomparison Project.

Results of PMIP2 coupled simulations of the mid-Holocene and Last Glacial Maximum, Part 2: feedbacks with emphasis on the location of the ITCZ and mid- and high latitudes heat budget

A set of coupled ocean-atmosphere(-vegetation) simulations using state of the art climate models is now available for the Last Glacial Maximum (LGM) and the Mid-Holocene (MH) through the second phase of the Paleoclimate Modeling Intercomparison Project (PMIP2). Here we quantify the latitudinal shift of the location of the Intertropical Convergence Zone (ITCZ) in the tropical regions during boreal summer and the change in precipitation in the northern part of the ITCZ. For both periods the shift is more pronounced over the continents and East Asia. The maritime continent is the region where the largest spread is found between models. We also clearly establish that the larger the increase in the meridional temperature gradient in the tropical Atlantic during summer at the MH, the larger the change in precipitation over West Africa. The vegetation feedback is however not as large as found in previous studies, probably due to model differences in the control simulation. Finally, we show that the feedback from snow and sea-ice at mid and high latitudes contributes for half of the cooling in the Northern Hemisphere for the LGM, with the remaining being achieved by the reduced CO2 and water vapour in the atmosphere. For the MH the snow and albedo feedbacks strengthen the spring cooling and enhance the boreal summer warming, whereas water vapour reinforces the late summer warming. These feedbacks are modest in the Southern Hemisphere. For the LGM most of the surface cooling is due to CO2 and water vapour.

Results of PMIP2 coupled simulations of the mid-Holocene and Last Glacial Maximum, Part 1: experiments and large-scale features

A set of coupled ocean-atmosphere simulations using state of the art climate models is now available for the Last Glacial Maximum and the Mid-Holocene through the second phase of the Paleoclimate Modeling Intercomparison Project (PMIP2). This study presents the large-scale features of the simulated climates and compares the new model results to those of the atmospheric models from the first phase of the PMIP, for which sea surface temperature was prescribed or computed using simple slab ocean formulations. We consider the large-scale features of the climate change, pointing out some of the major differences between the different sets of experiments. We show in particular that systematic differences between PMIP1 and PMIP2 simulations are due to the interactive ocean, such as the amplification of the African monsoon at the Mid-Holocene or the change in precipitation in mid-latitudes at the LGM. Also the PMIP2 simulations are in general in better agreement with data than PMIP1 simulations.

A systematic approach to identify the sources of tropical SST errors in coupled models using the adjustment of initialised experiments

Understanding the sources of systematic errors in climate models is challenging because of coupled feedbacks and errors compensation. The developing seamless approach proposes that the identification and the correction of short term climate model errors have the potential to improve the modeled climate on longer time scales. In previous studies, initialised atmospheric simulations of a few days have been used to compare fast physics processes (convection, cloud processes) among models. The present study explores how initialised seasonal to decadal hindcasts (re-forecasts) relate transient week-to-month errors of the ocean and atmospheric components to the coupled model long-term pervasive SST errors. A protocol is designed to attribute the SST biases to the source processes. It includes five steps: (1) identify and describe biases in a coupled stabilized simulation, (2) determine the time scale of the advent of the bias and its propagation, (3) find the geographical origin of the bias, (4) evaluate the degree of coupling in the development of the bias, (5) find the field responsible for the bias. This strategy has been implemented with a set of experiments based on the initial adjustment of initialised simulations and exploring various degrees of coupling. In particular, hindcasts give the time scale of biases advent, regionally restored experiments show the geographical origin and ocean-only simulations isolate the field responsible for the bias and evaluate the degree of coupling in the bias development. This strategy is applied to four prominent SST biases of the IPSLCM5A-LR coupled model in the tropical Pacific, that are largely shared by other coupled models, including the Southeast Pacific warm bias and the equatorial cold tongue bias. Using the proposed protocol, we demonstrate that the East Pacific warm bias appears in a few months and is caused by a lack of upwelling due to too weak meridional coastal winds off Peru. The cold equatorial bias, which surprisingly takes 30 years to develop, is the result of an equatorward advection of midlatitude cold SST errors. Despite large development efforts, the current generation of coupled models shows only little improvement. The strategy proposed in this study is a further step to move from the current random ad hoc approach, to a bias-targeted, priority setting, systematic model development approach.

Heme oxygenase-1 regulates cell proliferation via carbon monoxide-mediated inhibition of T-type Ca2+ channels

Induction of the antioxidant enzyme heme oxygenase-1 (HO-1) affords cellular protection and suppresses proliferation of vascular smooth muscle cells (VSMCs) associated with a variety of pathological cardiovascular conditions including myocardial infarction and vascular injury. However, the underlying mechanisms are not fully understood. Over-expression of Cav3.2 T-type Ca2+ channels in HEK293 cells raised basal [Ca2+]i and increased proliferation as compared with non-transfected cells. Proliferation and [Ca2+]i levels were reduced to levels seen in non-transfected cells either by induction of HO-1 or exposure of cells to the HO-1 product, carbon monoxide (CO) (applied as the CO releasing molecule, CORM-3). In the aortic VSMC line A7r5, proliferation was also inhibited by induction of HO-1 or by exposure of cells to CO, and patch-clamp recordings indicated that CO inhibited T-type (as well as L-type) Ca2+ currents in these cells. Finally, in human saphenous vein smooth muscle cells, proliferation was reduced by T-type channel inhibition or by HO-1 induction or CO exposure. The effects of T-type channel blockade and HO-1 induction were non-additive. Collectively, these data indicate that HO-1 regulates proliferation via CO-mediated inhibition of T-type Ca2+ channels. This signalling pathway provides a novel means by which proliferation of VSMCs (and other cells) may be regulated therapeutically.

Diverse mechanisms underlying the regulation of ion channels by carbon monoxide

Carbon monoxide is firmly established as an important, physiological signalling molecule as well as a potent toxin. Through its ability to bind metal-containing proteins it is known to interfere with a number of intracellular signalling pathways, and such actions can account for its physiological and pathological effects. In particular, CO can modulate the intracellular production of reactive oxygen species, nitric oxide and cGMP levels, as well as regulate MAP kinase signalling. In this review, we consider ion channels as more recently discovered effectors of CO signalling. CO is now known to regulate a growing number of different ion channel types, and detailed studies of the underlying mechanisms of action are revealing unexpected findings. For example, there are clear areas of contention surrounding its ability to increase the activity of high conductance, Ca2+ -sensitive K+ channels. More recent studies have revealed the ability of CO to inhibit T-type Ca2+ channels and have unveiled a novel signalling pathway underlying tonic regulation of this channel. It is clear that the investigation of ion channels as effectors of CO signalling is in its infancy, and much more work is required to fully understand both the physiological and the toxic actions of this gas. Only then can its emerging use as a therapeutic tool be fully and safely exploited.

Coupled versus uncoupled hindcast simulations of the Madden-Julian oscillation in the Year of Tropical Convection

This study investigates the impact of a full interactive ocean on daily initialised 15 day hindcasts of the Madden-Julian oscillation (MJO), measured against a Met Office Unified Model (MetUM) atmosphere control simulation (AGCM) during a 3 month period of the Year of Tropical Convection (YOTC). Results indicated that the coupled configuration (CGCM) extends MJO predictability over that of the AGCM, by up to 3-5 days. Propagation is improved in the CGCM, which we partly attribute to a more realistic phase relationship between sea surface temperature (SST) and convection. In addition, the CGCM demonstrates skill in representing downwelling oceanic Kelvin and Rossby waves which warm SSTs along their trajectory, with the potential to feed back on the atmosphere. These results imply that an ocean model capable of simulating internal ocean waves may be required to capture the full effect of air-sea coupling for the MJO.

Nonpsychotropic plant cannabinoids, cannabidivarin (CBDV) and cannabidiol (CBD), activate and desensitize transient receptor potential vanilloid 1 (TRPV1) channels in vitro: potential for the treatment of neuronal hyperexcitability

Epilepsy is the most common neurological disorder, with over 50 million people worldwide affected. Recent evidence suggests that the transient receptor potential cation channel subfamily V member 1 (TRPV1) may contribute to the onset and progression of some forms of epilepsy. Since the two nonpsychotropic cannabinoids cannabidivarin (CBDV) and cannabidiol (CBD) exert anticonvulsant activity in vivo and produce TRPV1-mediated intracellular calcium elevation in vitro, we evaluated the effects of these two compounds on TRPV1 channel activation and desensitization and in an in vitro model of epileptiform activity. Patch clamp analysis in transfected HEK293 cells demonstrated that CBD and CBDV dose-dependently activate and rapidly desensitize TRPV1, as well as TRP channels of subfamily V type 2 (TRPV2) and subfamily A type 1 (TRPA1). TRPV1 and TRPV2 transcripts were shown to be expressed in rat hippocampal tissue. When tested on epileptiform neuronal spike activity in hippocampal brain slices exposed to a Mg2+-free solution using multielectrode arrays (MEAs), CBDV reduced both epileptiform burst amplitude and duration. The prototypical TRPV1 agonist, capsaicin, produced similar, although not identical effects. Capsaicin, but not CBDV, effects on burst amplitude were reversed by IRTX, a selective TRPV1 antagonist. These data suggest that CBDV antiepileptiform effects in the Mg2+-free model are not uniquely mediated via activation of TRPV1. However, TRPV1 was strongly phosphorylated (and hence likely sensitized) in Mg2+-free solution-treated hippocampal tissue, and both capsaicin and CBDV caused TRPV1 dephosphorylation, consistent with TRPV1 desensitization. We propose that CBDV effects on TRP channels should be studied further in different in vitro and in vivo models of epilepsy.

Exogenous alpha-Synuclein decreases raft partitioning of Cav2.2 channels inducing dopamine release

alpha-Synuclein is thought to regulate neurotransmitter release through multiple interactions with presynaptic proteins, cytoskeletal elements, ion channels, and synaptic vesicles membrane. alpha-Synuclein is abundant in the presynaptic compartment, and its release from neurons and glia has been described as responsible for spreading of alpha-synuclein-derived pathology. alpha-Synuclein-dependent dysregulation of neurotransmitter release might occur via its action on surface-exposed calcium channels. Here, we provide electrophysiological and biochemical evidence to show that alpha-synuclein, applied to rat neurons in culture or striatal slices, selectively activates Cav2.2 channels, and said activation correlates with increased neurotransmitter release. Furthermore, in vivo perfusion of alpha-synuclein into the striatum also leads to acute dopamine release. We further demonstrate that alpha-synuclein reduces the amount of plasma membrane cholesterol and alters the partitioning of Cav2.2 channels, which move from raft to cholesterol-poor areas of the plasma membrane. We provide evidence for a novel mechanism through which alpha-synuclein acts from the extracellular milieu to modulate neurotransmitter release and propose a unifying hypothesis for the mechanism of alpha-synuclein action on multiple targets: the reorganization of plasma membrane microdomains.

Simulation of the global ENSO–Tropical cyclone teleconnection by a high-resolution coupled general circulation model

This study assesses the influence of the El Niño–Southern Oscillation (ENSO) on global tropical cyclone activity using a 150-yr-long integration with a high-resolution coupled atmosphere–ocean general circulation model [High-Resolution Global Environmental Model (HiGEM); with N144 resolution: ~90 km in the atmosphere and ~40 km in the ocean]. Tropical cyclone activity is compared to an atmosphere-only simulation using the atmospheric component of HiGEM (HiGAM). Observations of tropical cyclones in the International Best Track Archive for Climate Stewardship (IBTrACS) and tropical cyclones identified in the Interim ECMWF Re-Analysis (ERA-Interim) are used to validate the models. Composite anomalies of tropical cyclone activity in El Niño and La Niña years are used. HiGEM is able to capture the shift in tropical cyclone locations to ENSO in the Pacific and Indian Oceans. However, HiGEM does not capture the expected ENSO–tropical cyclone teleconnection in the North Atlantic. HiGAM shows more skill in simulating the global ENSO–tropical cyclone teleconnection; however, variability in the Pacific is overpronounced. HiGAM is able to capture the ENSO–tropical cyclone teleconnection in the North Atlantic more accurately than HiGEM. An investigation into the large-scale environmental conditions, known to influence tropical cyclone activity, is used to further understand the response of tropical cyclone activity to ENSO in the North Atlantic and western North Pacific. The vertical wind shear response over the Caribbean is not captured in HiGEM compared to HiGAM and ERA-Interim. Biases in the mean ascent at 500 hPa in HiGEM remain in HiGAM over the western North Pacific; however, a more realistic low-level vorticity in HiGAM results in a more accurate ENSO–tropical cyclone teleconnection.

Sensitivity of simulated regional Arctic climate to the choice of coupled model domain

The climate over the Arctic has undergone changes in recent decades. In order to evaluate the coupled response of the Arctic system to external and internal forcing, our study focuses on the estimation of regional climate variability and its dependence on large-scale atmospheric and regional ocean circulations. A global ocean–sea ice model with regionally high horizontal resolution is coupled to an atmospheric regional model and global terrestrial hydrology model. This way of coupling divides the global ocean model setup into two different domains: one coupled, where the ocean and the atmosphere are interacting, and one uncoupled, where the ocean model is driven by prescribed atmospheric forcing and runs in a so-called stand-alone mode. Therefore, selecting a specific area for the regional atmosphere implies that the ocean–atmosphere system can develop ‘freely’ in that area, whereas for the rest of the global ocean, the circulation is driven by prescribed atmospheric forcing without any feedbacks. Five different coupled setups are chosen for ensemble simulations. The choice of the coupled domains was done to estimate the influences of the Subtropical Atlantic, Eurasian and North Pacific regions on northern North Atlantic and Arctic climate. Our simulations show that the regional coupled ocean–atmosphere model is sensitive to the choice of the modelled area. The different model configurations reproduce differently both the mean climate and its variability. Only two out of five model setups were able to reproduce the Arctic climate as observed under recent climate conditions (ERA-40 Reanalysis). Evidence is found that the main source of uncertainty for Arctic climate variability and its predictability is the North Pacific. The prescription of North Pacific conditions in the regional model leads to significant correlation with observations, even if the whole North Atlantic is within the coupled model domain. However, the inclusion of the North Pacific area into the coupled system drastically changes the Arctic climate variability to a point where the Arctic Oscillation becomes an ‘internal mode’ of variability and correlations of year-to-year variability with observational data vanish. In line with previous studies, our simulations provide evidence that Arctic sea ice export is mainly due to ‘internal variability’ within the Arctic region. We conclude that the choice of model domains should be based on physical knowledge of the atmospheric and oceanic processes and not on ‘geographic’ reasons. This is particularly the case for areas like the Arctic, which has very complex feedbacks between components of the regional climate system.

Hydrogen sulfide inhibits Cav3.2 T-type Ca2+ channels

The importance of H2S as a physiological signaling molecule continues to develop, and ion channels are emerging as a major family of target proteins through which H2S exerts many actions. The purpose of the present study was to investigate its effects on T-type Ca2+ channels. Using patch-clamp electrophysiology, we demonstrate that the H2S donor, NaHS (10 μM-1 mM) selectively inhibits Cav3.2 T-type channels heterologously expressed in HEK293 cells, whereas Cav3.1 and Cav3.3 channels were unaffected. The sensitivity of Cav3.2 channels to H2S required the presence of the redox-sensitive extracellular residue H191, which is also required for tonic binding of Zn2+ to this channel. Chelation of Zn2+ with N,N,N',N'-tetra-2-picolylethylenediamine prevented channel inhibition by H2S and also reversed H2S inhibition when applied after H2S exposure, suggesting that H2S may act via increasing the affinity of the channel for extracellular Zn2+ binding. Inhibition of native T-type channels in 3 cell lines correlated with expression of Cav3.2 and not Cav3.1 channels. Notably, H2S also inhibited native T-type (primarily Cav3.2) channels in sensory dorsal root ganglion neurons. Our data demonstrate a novel target for H2S regulation, the T-type Ca2+ channel Cav3.2, and suggest that such modulation cannot account for the pronociceptive effects of this gasotransmitter.

Diverse mechanisms underlying the regulation of ion channels by carbon monoxide

Carbon monoxide (CO) is firmly established as an important, physiological signalling molecule as well as a potent toxin. Through its ability to bind metal-containing proteins, it is known to interfere with a number of intracellular signalling pathways, and such actions can account for its physiological and pathological effects. In particular, CO can modulate the intracellular production of reactive oxygen species, NO and cGMP levels, as well as regulate MAPK signalling. In this review, we consider ion channels as more recently discovered effectors of CO signalling. CO is now known to regulate a growing number of different ion channel types, and detailed studies of the underlying mechanisms of action are revealing unexpected findings. For example, there are clear areas of contention surrounding its ability to increase the activity of high conductance, Ca2+ -sensitive K+ channels. More recent studies have revealed the ability of CO to inhibit T-type Ca2+ channels and have unveiled a novel signalling pathway underlying tonic regulation of this channel. It is clear that the investigation of ion channels as effectors of CO signalling is in its infancy, and much more work is required to fully understand both the physiological and the toxic actions of this gas. Only then can its emerging use as a therapeutic tool be fully and safely exploited.

Ensemble downscaling in coupled solar wind-magnetosphere modeling for space weather forecasting

Advanced forecasting of space weather requires simulation of the whole Sun-to-Earth system, which necessitates driving magnetospheric models with the outputs from solar wind models. This presents a fundamental difficulty, as the magnetosphere is sensitive to both large-scale solar wind structures, which can be captured by solar wind models, and small-scale solar wind “noise,” which is far below typical solar wind model resolution and results primarily from stochastic processes. Following similar approaches in terrestrial climate modeling, we propose statistical “downscaling” of solar wind model results prior to their use as input to a magnetospheric model. As magnetospheric response can be highly nonlinear, this is preferable to downscaling the results of magnetospheric modeling. To demonstrate the benefit of this approach, we first approximate solar wind model output by smoothing solar wind observations with an 8 h filter, then add small-scale structure back in through the addition of random noise with the observed spectral characteristics. Here we use a very simple parameterization of noise based upon the observed probability distribution functions of solar wind parameters, but more sophisticated methods will be developed in the future. An ensemble of results from the simple downscaling scheme are tested using a model-independent method and shown to add value to the magnetospheric forecast, both improving the best estimate and quantifying the uncertainty. We suggest a number of features desirable in an operational solar wind downscaling scheme.