6 research outputs found
Computational and Experimental Investigation of Li-Doped Ionic Liquid Electrolytes: [pyr14][TFSI], [pyr13][FSI], and [EMIM][BF<sub>4</sub>]
We employ molecular dynamics (MD)
simulation and experiment to
investigate the structure, thermodynamics, and transport of <i>N</i>-methyl-<i>N</i>-butylpyrrolidinium bis(trifluoromethylsufonyl)imide
([pyr14][TFSI]), <i>N</i>-methyl-<i>N</i>-propylpyrrolidinium
bis(fluorosufonyl)imide ([pyr13][FSI]), and 1-ethyl-3-methylimidazolium
boron tetrafluoride ([EMIM][BF<sub>4</sub>]), as a function of Li-salt
mole fraction (0.05 ≤ <i>x</i><sub>Li<sup>+</sup></sub> ≤ 0.33) and temperature (298 K ≤ <i>T</i> ≤ 393 K). Structurally, Li<sup>+</sup> is shown to be solvated
by three anion neighbors in [pyr14][TFSI] and four anion neighbors
in both [pyr13][FSI] and [EMIM][BF<sub>4</sub>], and at all levels
of <i>x</i><sub>Li<sup>+</sup></sub> we find the presence
of lithium aggregates. Pulsed field gradient spin-echo NMR measurements
of diffusion and electrochemical impedance spectroscopy measurements
of ionic conductivity are made for the neat ionic liquids as well
as 0.5 molal solutions of Li-salt in the ionic liquids. Bulk ionic
liquid properties (density, diffusion, viscosity, and ionic conductivity)
are obtained with MD simulations and show excellent agreement with
experiment. While the diffusion exhibits a systematic decrease with
increasing <i>x</i><sub>Li<sup>+</sup></sub>, the contribution
of Li<sup>+</sup> to ionic conductivity increases until reaching a
saturation doping level of <i>x</i><sub>Li<sup>+</sup></sub> = 0.10. Comparatively, the Li<sup>+</sup> conductivity of [pyr14][TFSI]
is an order of magnitude lower than that of the other liquids, which
range between 0.1 and 0.3 mS/cm. Our transport results also demonstrate
the necessity of long MD simulation runs (∼200 ns) to converge
transport properties at room temperature. The differences in Li<sup>+</sup> transport are reflected in the residence times of Li<sup>+</sup> with the anions (τ<sup>Li/–</sup>), which are
revealed to be much larger for [pyr14][TFSI] (up to 100 ns at the
highest doping levels) than in either [EMIM][BF<sub>4</sub>] or [pyr13][FSI].
Finally, to comment on the relative kinetics of Li<sup>+</sup> transport
in each liquid, we find that while the net motion of Li<sup>+</sup> with its solvation shell (vehicular) significantly contributes to
net diffusion in all liquids, the importance of transport through
anion exchange increases at high <i>x</i><sub>Li<sup>+</sup></sub> and in liquids with large anions
Soluble Aβ induces prolonged efflux of K<sup>+</sup> in Tg2576 cortical neurons.
<p>Treatment with 1 µM Aβ<sub>1-40</sub> triggered rapid efflux of K<sup>+</sup> from Tg2576 neurons (A), which continued over the 120 minutes of recording. Aβ<sub>1-40</sub> treatment caused a rapid influx of H<sup>+</sup> in Tg2576 neurons (B), which did not stabilise over the 120 minute recording period.</p
Uptake of soluble Aβ by wildtype and Tg2576 cortical neurons <i>in vitro</i>.
<p>Wildtype and Tg2576 cortical neurons were treated with 10 µM of monomeric Aβ<sub>1-40</sub>, and immunostained for Aβ after 24 hours. In untreated Tg2576 neurons, Aβ was smoothly distributed throughout the cytoplasm and processes of all neurons (A). When Aβ<sub>1-40</sub> was applied to wildtype neurons, it was internalised and distributed in a punctate manner within the cytoplasm and processes (B). Notably, not all wildtype neurons internalised Aβ<sub>1-40</sub> (B). When Aβ<sub>1-40</sub> was applied to Tg2576 neurons, both smooth and punctately distributed Aβ was detected within neurons (C). scale bar = 25 µm.</p
Tg2576 cortical neurons are more vulnerable to soluble Aβ-induced neurotoxicity.
<p>Wildtype and Tg2576 cortical neurons were treated daily with 1 µM (A) or 10 µM (B) of monomeric Aβ<sub>1-40</sub> for 6 days, and neuronal viability (intracellular metabolism as assessed by Alamar Blue assay) assessed every 24 hours. At 1 µM concentrations, only Tg2576 neurons were vulnerable to Aβ<sub>1-40</sub>, resulting in approximately 30% cell death after 6 days (A). 10 µM Aβ<sub>1-40</sub> was mildly toxic to wildtype neurons over the experimental timecourse, but killed 40% of Tg2576 neurons after 6 days (B). The Alamar Blue neurotoxicity assay produced similar results to direct counting of dying cells via propidium iodide uptake following treatment with 10 µM Aβ<sub>1-40</sub> (C). * - p<0.05, ANOVA. Error bars represent standard error values from at least three replicates per experimental condition. This graph is representative of the results observed from 4 different experiments.</p
Soluble Aβ triggers caspase-3 expression in Tg2576 cortical neurons.
<p>Tg2576 neurons cultured for 14 days <i>in vitro</i> (DIV) showed no signs of caspase-3 activation (A). However, when 7 DIV Tg2576 neurons were treated with 1 µM Aβ<sub>1-40</sub> daily for 6 days, a substantial number of neurons were found to express caspase-3 (B).</p
Soluble Aβ causes disruptions in tau distribution in Tg2576 cortical neurons.
<p>Tau immunolabelling of the axonal cytoskeleton demonstrated that axonal morphology was similar between wildtype (A) and Tg2576 (B) cortical neurons over 7–14 DIV. Six daily 1 µM Aβ<sub>1-40</sub> treatments of 7DIV wildtype neurons had no discernible effect upon axonal morphology (C). However, substantial changes in tau-labelling were observed in Aβ<sub>1-40</sub> treated Tg2576 neurons (D); including increased intensity of tau immunostaining after 24 hours, followed by blebbing and axonal fragmentation which worsened after four days of treatment (D). Furthermore, after four consecutive days of 1 µM Aβ<sub>1-40</sub> treatment a number of axonal swellings, with dense accumulations of hyperphosphorylated tau, were observed in Tg2576 neuron cultures (E). scale bars = 30 µm (A–D), 15 µm (E).</p