Indium Tin Oxide@Carbon Core–Shell Nanowire and Jagged Indium Tin Oxide Nanowire

This paper reports two new indium tin oxide (ITO)-based nanostructures, namely ITO@carbon core–shell nanowire and jagged ITO nanowire. The ITO@carbon core–shell nanowires (~50 nm in diameter, 1–5 μm in length,) were prepared by a chemical vapor deposition process from commercial ITO nanoparticles. A carbon overlayer (~5–10 in thickness) was observed around ITO nanowire core, which was in situ formed by the catalytic decomposition of acetylene gas. This carbon overlayer could be easily removed after calcination in air at an elevated temperature of 700°C, thus forming jagged ITO nanowires (~40–45 nm in diameter). The growth mechanisms of ITO@carbon core–shell nanowire and jagged ITO nanowire were also suggested

Alterations in ethanol-induced behaviors and consumption in knock-in mice expressing ethanol-resistant NMDA receptors

Ethanol's action on the brain likely reflects altered function of key ion channels such as glutamatergic N-methyl-D-aspartate receptors (NMDARs). In this study, we determined how expression of a mutant GluN1 subunit (F639A) that reduces ethanol inhibition of NMDARs affects ethanol-induced behaviors in mice. Mice homozygous for the F639A allele died prematurely while heterozygous knock-in mice grew and bred normally. Ethanol (44 mM; ∼0.2 g/dl) significantly inhibited NMDA-mediated EPSCs in wild-type mice but had little effect on responses in knock-in mice. Knock-in mice had normal expression of GluN1 and GluN2B protein across different brain regions and a small reduction in levels of GluN2A in medial prefrontal cortex. Ethanol (0.75-2.0 g/kg; IP) increased locomotor activity in wild-type mice but had no effect on knock-in mice while MK-801 enhanced activity to the same extent in both groups. Ethanol (2.0 g/kg) reduced rotarod performance equally in both groups but knock-in mice recovered faster following a higher dose (2.5 g/kg). In the elevated zero maze, knock-in mice had a blunted anxiolytic response to ethanol (1.25 g/kg) as compared to wild-type animals. No differences were noted between wild-type and knock-in mice for ethanol-induced loss of righting reflex, sleep time, hypothermia or ethanol metabolism. Knock-in mice consumed less ethanol than wild-type mice during daily limited-access sessions but drank more in an intermittent 24 h access paradigm with no change in taste reactivity or conditioned taste aversion. Overall, these data support the hypothesis that NMDA receptors are important in regulating a specific constellation of effects following exposure to ethanol. © 2013 den Hartog et al