Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HTreceptor signaling-0

in the absence and presence of 50 mM KCl and/or drugs. Drugs were present as indicated during "Pretreat" and "50 mM KCl" incubations but not during the "Basal" incubation. Data is presented as the mean ± S.E.M. and the number of wells tested is indicated in parentheses. An asterisk indicates a significant difference (p < 0.05) between the transmitter release from control cells and from cells treated with calcium channel blockers. Potassium-stimulated release of glutamate was inhibited by 1 μM ω-Aga TK, 1 μM ω-Cgtx GVIA and 1 μM nimodipine while basal glutamate release was not altered (Panel A). Potassium-stimulated release of CGRP was inhibited by 1 μM ω-Aga TK, 1 μM ω-Cgtx GVIA and 1 μM nimodipine while basal CGRP release was not altered (Panel B).<p><b>Copyright information:</b></p><p>Taken from "Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HTreceptor signaling"</p><p>http://www.molecularpain.com/content/4/1/12</p><p>Molecular Pain 2008;4():12-12.</p><p>Published online 16 Apr 2008</p><p>PMCID:PMC2359740.</p><p></p

Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HTreceptor signaling-3

in the absence and presence of 50 mM KCl and/or drugs. Drugs were present as indicated during "Pretreat" and "50 mM KCl" incubations but not during the "Basal" incubation. Data is presented as the mean ± S.E.M. and the number of wells tested is indicated in parentheses. An asterisk indicates a significant difference (p < 0.05) between the transmitter release from control cells and from cells treated with calcium channel blockers. Potassium-stimulated release of glutamate was inhibited by 1 μM ω-Aga TK, 1 μM ω-Cgtx GVIA and 1 μM nimodipine while basal glutamate release was not altered (Panel A). Potassium-stimulated release of CGRP was inhibited by 1 μM ω-Aga TK, 1 μM ω-Cgtx GVIA and 1 μM nimodipine while basal CGRP release was not altered (Panel B).<p><b>Copyright information:</b></p><p>Taken from "Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HTreceptor signaling"</p><p>http://www.molecularpain.com/content/4/1/12</p><p>Molecular Pain 2008;4():12-12.</p><p>Published online 16 Apr 2008</p><p>PMCID:PMC2359740.</p><p></p

Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HTreceptor signaling-1

Ions in the absence and presence of 50 mM KCl and/or drugs. Drugs were present as indicated during "Pretreat" and "50 mM KCl" incubations but not during the "Basal" incubation. Data is presented as the mean ± S.E.M. and the number of wells tested is indicated in parentheses. An asterisk indicates a significant difference (p < 0.05) between the transmitter release from control cells and from cells treated with serotonin and/or pertussis toxin. Serotonin (10 μM) inhibits KCl-stimulated but not basal release of glutamate (Panel A). Overnight pertussis toxin treatment (100 ng/ml) blocks the serotonergic inhibition of KCl-stimulated glutamate release without affecting basal or KCl-stimulated release. Serotonin (10 μM) inhibits KCl-stimulated but not basal release of CGRP (Panel B). Overnight pertussis toxin treatment (100 ng/ml) blocks the serotonergic inhibition of KCl-stimulated CGRP release without affecting basal or KCl-stimulated release from trigeminal neurons. Serotonin inhibits KCl-stimulated release of CGRP from trigeminal neurons from female rats in the absence and presence of the calcium channel blockers, 1 μM ω-Cgtx GVIA and 1 μM nimodine to a similar extent (Panel C). Serotonin (1 μM) reversibly inhibits calcium current amplitude (Panel D). Peak currents were plotted against time for this cell. The trigeminal neurons were depolarized to 0 mV for 100 msec every 20 seconds from a holding potential of -80 mV. The horizontal bar indicates perfusion of 1 μM 5-HT. Inset, superimposed current traces from the indicated time points.<p><b>Copyright information:</b></p><p>Taken from "Release of glutamate and CGRP from trigeminal ganglion neurons: Role of calcium channels and 5-HTreceptor signaling"</p><p>http://www.molecularpain.com/content/4/1/12</p><p>Molecular Pain 2008;4():12-12.</p><p>Published online 16 Apr 2008</p><p>PMCID:PMC2359740.</p><p></p

Förster Resonance Energy Transfer-Based Biosensing Platform with Ultrasmall Silver Nanoclusters as Energy Acceptors

We studied the energy transfer (ET) property of ultrasmall Ag nanoclusters (Ag NCs) and exploited its biosensing application for the first time. A hybridized DNA duplex model was designed to study the energy transfer process from fluorescent energy donors to Ag NCs. By changing the DNA duplex model and the number of hybridized pairs, the separation distance between the energy donor and Ag NCs was adjusted to investigate the distance dependence and possible mechanisms involved in the ET process, which was assigned to Förster resonance energy transfer (FRET). Using Ag NCs with different photophysical properties as energy acceptors, FRET-based biosensing platforms with two different energy donors were constructed utilizing either the off–on or ratiometric fluorescence signaling. This study will provide the basis for understanding energy transfer properties of Ag NCs and bring to light the universal application of these properties in bio/chemo sensing

Effect of Small-Scale Turbulence on the Physiology and Morphology of Two Bloom-Forming Cyanobacteria

<div><p>The main goal of the present work is to test the hypothesis that small-scale turbulence affected physiological activities and the morphology of cyanobacteria in high turbulence environments. Using quantified turbulence in a stirring device, we conducted one set of experiments on cultures of two strains of cyanobacteria with different phenotypes; i.e., unicellular <i>Microcystis flos-aquae</i> and colonial <i>Anabaena flos-aquae</i>. The effect of small-scale turbulence examined varied from 0 to 8.01×10⁻² m²s^-3, covering the range of turbulence intensities experienced by cyanobacteria in the field. The results of photosynthesis activity and the cellular chlorophyll <i>a</i> in both strains did not change significantly among the turbulence levels, indicating that the potential indirect effects of a light regime under the gradient of turbulent mixing could be ignored. However, the experiments demonstrated that small-scale turbulence significantly modulated algal nutrient uptake and growth in comparison to the stagnant control. Cellular N and C of the two stains showed approximately the same responses, resulting in a similar pattern of C/N ratios. Moreover, the change in the phosphate uptake rate was similar to that of growth in two strains, which implied that growth characteristic responses to turbulence may be dependent on the P strategy, which was correlated with accumulation of polyphosphate. Additionally, our results also showed the filament length of <i>A</i>. <i>flos-aquae</i> decreased in response to high turbulence, which could favor enhancement of the nutrient uptake. These findings suggested that both <i>M</i>. <i>flos-aquae</i> and <i>A</i>. <i>flos-aquae</i> adjust their growth rates in response to turbulence levels in the ways of asynchronous cellular stoichiometry of C, N, and P, especially the phosphorus strategy, to improve the nutrient application efficiency. The fact that adaptation strategies of cyanobacteria diversely to turbulence depending on their physiological conditions presents a good example to understand the direct cause—effect relationship between hydrodynamic forces and algae.</p></div

Cellular stoichiometry of <i>M</i>. <i>flos-aquae</i> and <i>A</i>. <i>flos-aquae</i> under different levels of turbulence in the logarithmic growth phase.

<p>Cellular stoichiometry of <i>M</i>. <i>flos-aquae</i> and <i>A</i>. <i>flos-aquae</i> under different levels of turbulence in the logarithmic growth phase.</p

Changes in the maximum electron transfer rate (ETR_max) (a), <i>F</i>_<i>v</i><i>/F</i>_<i>m</i> (b) and cellular chlorophyll <i>a</i> (<i>Chla</i>) (c) of <i>M</i>. <i>flos-aquae</i> and <i>A</i>. <i>flos-aquae</i> at different turbulent dissipation rate levels in the logarithmic growth phase. The data are the mean ± SD (n = 3).

<p>Changes in the maximum electron transfer rate (ETR_max) (a), <i>F</i>_<i>v</i><i>/F</i>_<i>m</i> (b) and cellular chlorophyll <i>a</i> (<i>Chla</i>) (c) of <i>M</i>. <i>flos-aquae</i> and <i>A</i>. <i>flos-aquae</i> at different turbulent dissipation rate levels in the logarithmic growth phase. The data are the mean ± SD (n = 3).</p

The specific growth rates of <i>M</i>. <i>flos-aquae</i> and <i>A</i>. <i>flos-aquae</i> under different levels of turbulence.

<p>The specific growth rates of <i>M</i>. <i>flos-aquae</i> and <i>A</i>. <i>flos-aquae</i> under different levels of turbulence.</p

Geometric dimensions of the reactor (Unit: mm).

<p>Geometric dimensions of the reactor (Unit: mm).</p

Turbulent dissipation rate and Kolmogorov microscale in different levels of rotation speed estimated by the CFD hydrodynamic model.

<p>Turbulent dissipation rate and Kolmogorov microscale in different levels of rotation speed estimated by the CFD hydrodynamic model.</p