Carbon monoxide and methanol oxidation at platinum catalysts supported on ordered mesoporous carbon: the influence of functionalization of the support.

The influence of different functionalization treatments of the support on the electrocatalytic activity towards CO and methanol oxidation at platinum nanoparticles deposited on ordered mesoporous carbons (OMC) has been studied for the first time. Before deposition of the metal, the carbon support was functionalized applying several procedures, with the purpose to generate oxygenated groups for anchoring the Pt nanoparticles by the formic acid (FM) and borohydride (BM) reduction methods. Good dispersion of the catalyst was obtained in all cases. It has been shown that particle size, and consequently the lattice parameter and metal surface area, depends on the functionalization treatment employed. CO and methanol electrooxidation was studied at all prepared catalysts applying cyclic voltammetry. It was observed that CO stripping occurs at more negative potentials (around 0.10-0.15 V) with these supports with respect to Vulcan XC-72 supported catalysts, and the best results for both methods were achieved with OMC functionalized with concentrated nitric acid for 0.5 h. This carbon support presents a higher amount of oxygenated groups without the loss of the ordered structure. In situ infrared studies have been performed for the first time with this type of catalyst, showing that the effect of the carbon support on the CO oxidation potential is similar to the presence of a second metal as Ru under the same experimental conditions. Methanol electrooxidation is also dependent on the nature of the support, as proved from both cyclic voltammetry and chronoamperometry. In this case, results depend on the method of nanoparticles preparation and seem to be better for BM.

Interaction between neuropeptide Y (NPY) and brain-derived neurotrophic factor in NPY-mediated neuroprotection against excitotoxicity: a role for microglia.

The neuroprotective effect of neuropeptide Y (NPY) receptor activation was investigated in organotypic mouse hippocampal slice cultures exposed to the glutamate receptor agonist alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). Exposure of 2-week-old slice cultures, derived from 7-day-old C57BL/6 mice, to 8 microm AMPA, for 24 h, induced degeneration of CA1 and CA3 pyramidal cells, as measured by cellular uptake of propidium iodide (PI). A significant neuroprotection, with a reduction of PI uptake in CA1 and CA3 pyramidal cell layers, was observed after incubation with a Y(2) receptor agonist [NPY(13-36), 300 nm]. This effect was sensitive to the presence of the selective Y(2) receptor antagonist (BIIE0246, 1 microm), but was not affected by addition of TrkB-Fc or by a neutralizing antibody against brain-derived neurotrophic factor (BDNF). Moreover, addition of a Y(1) receptor antagonist (BIBP3226, 1 microm) or a NPY-neutralizing antibody helped to disclose a neuroprotective role of endogenous NPY in CA1 region. Cultures exposed to 8 microm AMPA for 24 h, displayed, as measured by an enzyme-linked immunosorbent assay, a significant increase in BDNF. In such cultures there was an up-regulation of neuronal TrkB immunoreactivity, as well as the presence of BDNF-immunoreactive microglial cells at sites of injury. Thus, an increase of AMPA-receptor mediated neurodegeneration, in the mouse hippocampus, was prevented by neuroprotective pathways activated by NPY receptors (Y(1) and Y(2)), which can be affected by BDNF released by microglia and neurons.