Importance of carbon-nitrogen interactions and ozone on ecosystem hydrology during the 21st century

Author Posting. © American Geophysical Union, 2009. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research 114 (2009): G01020, doi:10.1029/2008JG000826.There is evidence that increasing CO2 concentrations have reduced evapotranspiration and increased runoff through reductions in stomatal conductance during the twentieth century. While this process will continue to counteract increased evapotranspiration associated with future warming, it is highly dependent upon concurrent changes in photosynthesis, especially due to CO2 fertilization, nitrogen limitation, and ozone exposure. A new version of the Terrestrial Ecosystem Model (TEM-Hydro) was developed to examine the effects of carbon and nitrogen on the water cycle. We used two climate models (NCAR CCSM3 and DOE PCM) and two emissions scenarios (SRES B1 and A2) to examine the effects of climate, elevated CO2, nitrogen limitation, and ozone exposure on the hydrological cycle in the eastern United States. While the direction of future runoff changes is largely dependent upon predicted precipitation changes, the effects of elevated CO2 on ecosystem function (stomatal closure and CO2 fertilization) increase runoff by 3–7%, as compared to the effects of climate alone. Consideration of nitrogen limitation and ozone damage on photosynthesis increases runoff by a further 6–11%. Failure to consider the effects of the interactions among nitrogen, ozone, and elevated CO2 may lead to significant regional underestimates of future runoff.This study was funded by the Interdisciplinary Science Program of the U.S. National Aeronautics and Space Administration (NNG04GJ80G, NNG04GM39G), the Dynamic Global Economic Modeling of Greenhouse Gas Emissions and Mitigation from Land-Use Activities of the U.S. Environmental Protection Agency (XA-83240101), and the Nonlinear Response to Global Change in Linked Aquatic and Terrestrial Ecosystems of the U.S. EPA (XA-83326101)

Seizures elevate gliovascular unit Ca2+ and cause sustained vasoconstriction

Seizures can result in a severe hypoperfusion/hypoxic attack that causes postictal memory and behavioral impairments. However, neither postictal changes to microvasculature nor Ca2+ changes in key cell types controlling blood perfusion have been visualized in vivo, leaving essential components of the underlying cellular mechanisms unclear. Here, we use 2-photon microvascular and Ca2+ imaging in awake mice to show that seizures result in a robust vasoconstriction of cortical penetrating arterioles, which temporally mirrors the prolonged postictal hypoxia. The vascular effect was dependent on cyclooxygenase 2, as pretreatment with ibuprofen prevented postictal vasoconstriction. Moreover, seizures caused a rapid elevation in astrocyte endfoot Ca2+ that was confined to the seizure period, and vascular smooth muscle cells displayed a significant increase in Ca2+ both during and following seizures, lasting up to 75 minutes. Our data show enduring postictal vasoconstriction and temporal activities of 2 cell types within the neurovascular unit that are associated with seizure-induced hypoperfusion/hypoxia. These findings support prevention of this event may be a novel and tractable treatment strategy in patients with epilepsy who experience extended postseizure impairments