• Proceedings of the Korean Vacuum Society Conference
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• 2012.02a
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• pp.218-218
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• 2012

Nanocrystalline $SnO_2$ colloids are synthesized by hydrolysis of $SnCl_4{\cdot}5H_2O$ in aqueous ammonia solution. The synthesized $SnO_2$ nanoparticles with ca. 15 nm in diameter are coated on a fluorinedoped thin oxide (FTO) conductive substrate and heated at $550^{\circ}C$. The annealed $SnO_2$ film is treated with aqueous $TiCl_4$ solution, which is sensitzied with MK-2 dye (2-cyano-3-[5'''-(9-ethyl- 9H-carbazol-3-yl)-3',3'',3''',4-tetra-n-hexyl-[2,2',5',2'',5'',2''']-quater thiophen-5-yl]). Compared to bare $SnO_2$ film, the conversion efficiency is significantly improved from 0.22% to 3.13% after surface treatment of $SnO_2$ with $TiCl_4$, which is mainly due to the large increases in both photocurrent density from 1.33 to $9.46mA/cm^2$ and voltage from 315 to 634 mV. It is noted that little change in the amount of the adsorbed dye is detected from 1.21 for the bare $SnO_2$ to $1.28{\mu}mol/cm^2$ for the $TiCl_{4-}$ treated $SnO_2$. This indicates that the photocurrent density increased by more than 6 times is not closely related to the dye loading concentration. From the photocurrent and voltage transient spectroscopic studies, electron life time increases by about 13 order of magnitude, whereas electron diffusion coefficient decreases by about 3.6 times after $TiCl_4$ treatment. Slow electron diffusion rate offers sufficient time for regeneration kinetics. As a result, charge collection efficiency of about 40% before $TiCl_4$ treatment is improved to 95% after $TiCl_4$ treatment. The large increase in voltage is due to the significant increase in electron life time, associated with upward shift of fermi energy.

• Biomolecules & Therapeutics
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• v.29 no.6
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• pp.630-636
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• 2021

Eupafolin, a constituent of the aerial parts of Phyla nodiflora, has neuroprotective property. Because reducing the synaptic release of glutamate is crucial to achieving pharmacotherapeutic effects of neuroprotectants, we investigated the effect of eupafolin on glutamate release in rat cerebrocortical synaptosomes and explored the possible mechanism. We discovered that eupafolin depressed 4-aminopyridine (4-AP)-induced glutamate release, and this phenomenon was prevented in the absence of extracellular calcium. Eupafolin inhibition of glutamate release from synaptic vesicles was confirmed through measurement of the release of the fluorescent dye FM 1-43. Eupafolin decreased 4-AP-induced [Ca²⁺]_i elevation and had no effect on synaptosomal membrane potential. The inhibition of P/Q-type Ca²⁺ channels reduced the decrease in glutamate release that was caused by eupafolin, and docking data revealed that eupafolin interacted with P/Q-type Ca²⁺ channels. Additionally, the inhibition of calcium/calmodulin-dependent protein kinase II (CaMKII) prevented the effect of eupafolin on evoked glutamate release. Eupafolin also reduced the 4-AP-induced activation of CaMK II and the subsequent phosphorylation of synapsin I, which is the main presynaptic target of CaMKII. Therefore, eupafolin suppresses P/Q-type Ca²⁺ channels and thereby inhibits CaMKII/synapsin I pathways and the release of glutamate from rat cerebrocortical synaptosomes.