Concordia University

About: Concordia University is a education organization based out in Montreal, Quebec, Canada. It is known for research contribution in the topics: Context (language use) & Control theory. The organization has 13565 authors who have published 31084 publications receiving 783525 citations. The organization is also known as: Sir George Williams University & Loyola College, Montreal.

Future changes in climate, ocean circulation, ecosystems, and biogeochemical cycling simulated for a business-as-usual CO2 emission scenario until year 4000 AD

Abstract: A new model of global climate, ocean circulation, ecosystems, and biogeochemical cycling, including a fully coupled carbon cycle, is presented and evaluated. The model is consistent with multiple observational data sets from the past 50 years as well as with the observed warming of global surface air and sea temperatures during the last 150 years. It is applied to a simulation of the coming two millennia following a business-as-usual scenario of anthropogenic CO2 emissions (SRES A2 until year 2100 and subsequent linear decrease to zero until year 2300, corresponding to a total release of 5100 GtC). Atmospheric CO2 increases to a peak of more than 2000 ppmv near year 2300 (that is an airborne fraction of 72% of the emissions) followed by a gradual decline to ∼1700 ppmv at year 4000 (airborne fraction of 56%). Forty-four percent of the additional atmospheric CO2 at year 4000 is due to positive carbon cycle–climate feedbacks. Global surface air warms by ∼10°C, sea ice melts back to 10% of its current area, and the circulation of the abyssal ocean collapses. Subsurface oxygen concentrations decrease, tripling the volume of suboxic water and quadrupling the global water column denitrification. We estimate 60 ppb increase in atmospheric N2O concentrations owing to doubling of its oceanic production, leading to a weak positive feedback and contributing about 0.24°C warming at year 4000. Global ocean primary production almost doubles by year 4000. Planktonic biomass increases at high latitudes and in the subtropics whereas it decreases at midlatitudes and in the tropics. In our model, which does not account for possible direct impacts of acidification on ocean biology, production of calcium carbonate in the surface ocean doubles, further increasing surface ocean and atmospheric pCO2. This represents a new positive feedback mechanism and leads to a strengthening of the positive interaction between climate change and the carbon cycle on a multicentennial to millennial timescale. Changes in ocean biology become important for the ocean carbon uptake after year 2600, and at year 4000 they account for 320 ppmv or 22% of the atmospheric CO2 increase since the preindustrial era.

Differential involvement of ventral tegmental mu, delta and kappa opioid receptors in modulation of basal mesolimbic dopamine release: in vivo microdialysis studies.

Abstract: In vivo microdialysis was used to assess the involvement of ventral tegmental area (VTA) mu, delta, and kappa opioid receptors in modulation of basal extracellular ventral striatal dopamine (DA) and DA-metabolite concentrations. Independent groups of chloral hydrate-anesthetized rats were given VTA microinjections of selective opioid agonists, and extracellular ventral striatal DA and DA-metabolite concentrations were assayed using HPLC. VTA microinjections of [D-Ala2, N-Me-Phe4-Gly5-ol]-enkephalin (DAMGO; a mu agonist) and [D-Pen2, D-Pen5]-enkephalin (DDDPE; a delta agonist) each caused dose-orderly increases in ventral striatal DA and DA-metabolite concentrations. The effective concentrations of DPDPE were 100- to 1000-fold higher than the effective concentrations of DAMGO. VTA microinjections of (trans-(dl)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclo-hexyl]- benzeneacetamide) methane sulfonate hydrate (U-50,488H); a kappa agonist) failed to alter ventral striatal DA concentrations at any dose tested, but subsequent systemic injections significantly decreased DA and DA-metabolite concentrations. Pretreatment with VTA microinjections of 17-cyclopropylmethyl-6,7-dehydro-4,5-epoxy-3,14-dihydroxy-6,7,2',3'- indolmorphinan hydrochloride (naltrindole; a delta antagonist) (delta antagonist) antagonized VTA DPDPE-mediated increases in ventral striatal DA and DA-metabolite concentrations but failed to antagonize VTA DAMGO-mediated increases. Pretreatment with D-Pen-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP; a mu antagonist) antagonized VTA DAMGO-mediated increases but failed to antagonize VTA DPDPE-mediated increases. Thus both mu and delta receptor agonist appear capable of increasing ventral striatal DA and DA-metabolite concentrations through selective actions on their preferred class of opioid receptors in the VTA. The increases in ventral striatal DA and DA-metabolite concentrations that are seen after systemic treatment with kappa opioid agonists appear not to involve VTA opioid receptors.