PubMed · 14981619
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Peter Gross. 2004. Functional Gitelman syndrome?. https://doi.org/10.1053/j.ajkd.2003.12.039
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We have used Monte Carlo simulations to understand the generation of quantal responses at the single active zones of CA1 synapses. We constructed a model of AMPA channel activation that accounts for the responses to controlled glutamate application and a model of glutamate diffusion in the synaptic cleft. With no further adjustments to these models, we simulated the response to the release of glutamate from a single vesicle. The predicted response closely matches the rise time of observed responses, which recent measurements show is much faster (<100 micros) than previously thought. The simulations show that initial channel opening is driven by a brief (<100 micros) glutamate spike near the site of vesicle fusion, producing a hotspot of channel activation (diameter: approximately 250 nm) smaller than many synapses. Quantal size therefore depends more strongly on the density of channels than their number, a finding that has important implications for measuring synaptic strength. Recent measurements allow estimation of AMPA receptor density at CA1 synapses. Using this value, our simulations correctly predicts a quantal amplitude of approximately 10 pA. We have also analyzed the properties of excitatory postsynaptic currents (EPSCs) generated by the multivesicular release that can occur during evoked responses. We find that summation is nearly linear and that the existence of multiple narrow peaks in amplitude histograms can be accounted for. It has been unclear how to reconcile the existence of these narrow peaks, which indicate that the variation of quantal amplitude is small (CV < 0.2) with the highly variable amplitude of miniature EPSCs (mEPSCs; CV approximately 0.6). According to one theory, mEPSC variability arises from variation in vesicle glutamate content. However, both our modeling results and recent experimental results indicate that this view cannot account for the observed rise time/amplitude correlation of mEPSCs. In contrast, this correlation and the high mEPSC variability can be accounted for if some mEPSCs are generated by two or more vesicles released with small temporal jitter. We conclude that a broad range of results can be accounted for by simple principles: quantal amplitude (approximately 10 pA) is stereotyped, some mEPSCs are multivesicular at moderate and large synapses, and evoked responses are generated by quasi-linear summation of multiple quanta.
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Previous sorption/desorption batch experiments have indicated that bentazone is weakly sorbed by soils. In addition, field experiments have shown that 4% of the bentazone sprayed can be leached to drainage water. In order to complete bentazone characterisation, we have assessed the effect of time on its behaviour in contrasting soils. In laboratory studies, bentazone was added to three topsoils (sandy, loamy and clay soils). Bentazone degradation, sorption/desorption kinetics and isotherm measurements were carried out at different times. At 160 days after treatment, bentazone mineralisation amounts varied from 2.1% (sandy soil) to 14% (clay soil). The extractable amounts became lower (from 97% after treatment to 12% after 160 days for the clay soil) and a greater number of desorption series was needed to obtain these products. Nevertheless, at the end of the experiments, a small amount of bentazone was still extracted by water. At the same time, bound residues of bentazone reached 65% in clay soil. Statistical analysis indicated effects of both residence time and soil type on bentazone behaviour.