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  • 1
    Electronic Resource
    Electronic Resource
    HERBICIDE CONTAMINATION BY THE 1993 GREAT FLOOD ALONG THE MISSISSIPPI RWER (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of the American Water Resources Association 34 (1998), S. 0 
    Details
    ISSN: 1752-1688
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Architecture, Civil Engineering, Surveying , Geography
    Notes: : The Great Flood of 1993 inundated more than 355,000 ha of illinois cropland, creating great concern for the possible contamination of farmland by herbicides. The objective of this study was to assess the herbicide contamination of floodwaters and farmland due to the great flood of 1993. Floodwater samples were collected between August 5 and December 20, 1993, at the Horseshoe Lake State Game Reserve in Alexander County, Illinois, USA. Water and suspended sediment were tested separately for the more commonly used herbicides in Illinois and the midwestern USA: alachior, atrazine, and cyanazine.These herbicides were detected in the floodwater samples, but concentrations were all below the health advisory concentration of 3 μg/L established for drinking water by the United States Environmental Protection Agency. No herbicides were detected in the suspended sediment.After the recession of the flood, soil samples from flooded and non-flooded corn fields were collected for comparison. Soil samples taken from two out of three sampling locations had a 0.4 to 0.8 μg/kg increase in atrazine at the flooded verses the non-flooded sites. Concentrations were 500 to 1,000 times lower than the recommended 1 mg/kg rate at which this herbicides typically applied to soil.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1752-1688.1998.tb00965.x
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  • 2
    Electronic Resource
    Electronic Resource
    Glutamate-induced elevations in intracellular chloride concentration in hippocampal cell cultures derived from EYFP-expressing mice (2004)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 19 (2004), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The homeostasis of intracellular Cl− concentration ([Cl−]i) is critical for neuronal function, including γ-aminobutyric acid (GABA)ergic synaptic transmission. Here, we investigated activity-dependent changes in [Cl−]i using a transgenetically expressed Cl−-sensitive enhanced yellow-fluorescent protein (EYFP) in cultures of mouse hippocampal neurons. Application of glutamate (100 µm for 3 min) in a bath perfusion to cell cultures of various days in vitro (DIV) revealed a decrease in EYFP fluorescence. The EYFP signal increased in amplitude with increasing DIV, reaching a maximal response after 7 DIV. Glutamate application resulted in a slight neuronal acidification. Although EYFP fluorescence is sensitive to pH, EYFP signals were virtually abolished in Cl−-free solution, demonstrating that the EYFP signal represented an increase in [Cl−]i. Similar to glutamate, a rise in [Cl−]i was also induced by specific ionotropic glutamate receptor agonists and by increasing extracellular [K+], indicating that an increase in driving force for Cl− suffices to increase [Cl−]i. To elucidate the membrane mechanisms mediating the Cl− influx, a series of blockers of ion channels and transporters were tested. The glutamate-induced increase in [Cl−]i was resistant to furosemide, bumetanide and 4,4′-diisothiocyanato-stilbene-2,2′-disulphonic acid (DIDS), was reduced by bicuculline to about 80% of control responses, and was antagonized by niflumic acid (NFA) and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB). We conclude that membrane depolarization increases [Cl−]i via several pathways involving NFA- and NPPB-sensitive anion channels and GABAA receptors, but not through furosemide-, bumetanide- or DIDS-sensitive Cl− transporters. The present study highlights the vulnerability of [Cl−]i homeostasis after membrane depolarization in neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.0953-816X.2004.03422.x
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