Applications of Plasmon-Enhanced Nanocatalysis to Organic Transformations.

Localized surface plasmon resonance (LSPR) is a physical phenomenon exhibited by nanoparticles of metals including coinage metals, alkali metals, aluminum, and some semiconductors which translates into electromagnetic, thermal, and chemical properties. In the past decade, LSPR has been taken advantage of in the context of catalysis. While plasmonic nanoparticles (PNPs) have been successfully applied toward enhancing catalysis of inorganic reactions such as water splitting, they have also demonstrated exciting performance in the catalysis of organic transformations with potential applications in synthesis of molecules from commodity to pharmaceutical compounds. The advantages of this approach include improved selectivity, enhanced reaction rates, and milder reaction conditions. This review provides the basics of LSPR theory, details the mechanisms at play in plasmon-enhanced nanocatalysis, sheds light onto such nanocatalyst design, and finally systematically presents the breadth of organic reactions hence catalyzed.

Enhancing Singlet Oxygen Photocatalysis with Plasmonic Nanoparticles.

Photocatalysts able to trigger the production of singlet oxygen species are the topic of intense research efforts in organic synthesis. Yet, challenges still exist in improving their activity and optimizing their use. Herein, we exploited the benefits of plasmonic nanoparticles to boost the activity of such photocatalysts via an antenna effect in the visible range. We synthesized silica-coated silver nanoparticles (Ag@SiO2 NPs), with silica shells which thicknesses ranged from 7 to 45 nm. We showed that they served as plasmonically active supports for tris(bipyridine)ruthenium(II), [Ru(bpy)3]2+, and demonstrated an enhanced catalytic activity under white light-emitting diode (LED) irradiation for citronellol oxidation, a key step in the commercial production of rose oxide fragrance. A maximum enhancement of the plasmon-mediated reactivity of approximately 3-fold was observed with a 28 nm silica layer along with a 4-fold enhancement in the emission intensity of the photocatalyst. Using electron energy loss spectroscopy (EELS) and boundary element method simulations, we mapped the decay of the plasmonic signal around the Ag core and provided a rationale for the observed catalytic enhancement. This work provides a systematic analysis of the promising properties of plasmonic NPs used as catalysis-enhancing supports for common homogeneous photocatalysts and a framework for the successful design of such systems in the context of organic transformations.

Modulation of transmitter release by presynaptic resting potential and background calcium levels.

Activation of presynaptic ion channels alters the membrane potential of nerve terminals, leading to changes in transmitter release. To study the relationship between resting potential and exocytosis, we combined pre- and postsynaptic electrophysiological recordings with presynaptic Ca(2+) measurements at the calyx of Held. Depolarization of the membrane potential to between -60 mV and -65 mV elicited P/Q-type Ca(2+) currents of < 1 pA and increased intraterminal Ca(2+) by < 100 nM. These small Ca(2+) elevations were sufficient to enhance the probability of transmitter release up to 2-fold, with no effect on the readily releasable pool of vesicles. Moreover, the effects of mild depolarization on release had slow kinetics and were abolished by 1 mM intraterminal EGTA, suggesting that Ca(2+) acted through a high-affinity binding site. Together, these studies suggest that control of resting potential is a powerful means for regulating synaptic function at mammalian synapses.

Estimate of the chloride concentration in a central glutamatergic terminal: a gramicidin perforated-patch study on the calyx of Held.

The function of presynaptic terminals is regulated by intracellular Cl-, the levels of which modify vesicular endocytosis and transmitter refilling and mediate the effects of presynaptic ligand-gated Cl- channels. Nevertheless, the concentration of Cl- in a central nerve terminal is unknown, and it is unclear whether terminals can regulate Cl- independently of the soma. Using perforated-patch recording in a mammalian synapse, we found that terminals accumulate Cl- up to 21 mm, between four and five times higher than in their parent cell bodies. Changing [Cl-] did not alter vesicular glutamate content in intact terminals, unlike in vitro experiments. Thus, glutamatergic terminals maintain an elevated Cl- concentration without compromising synaptic transmission.

Retroinhibition of presynaptic Ca2+ currents by endocannabinoids released via postsynaptic mGluR activation at a calyx synapse.

We investigated the mechanisms by which activation of group I metabotropic glutamate receptors (mGluRs) and CB1 cannabinoid receptors (CB1Rs) leads to inhibition of synaptic currents at the calyx of Held synapse in the medial nucleus of the trapezoid body (MNTB) of the rat auditory brainstem. In approximately 50% of the MNTB neurons tested, activation of group I mGluRs by the specific agonist (s)-3,5-dihydroxyphenylglycine (DHPG) reversibly inhibited AMPA receptor- and NMDA receptor-mediated EPSCs to a similar extent and reduced paired-pulse depression, suggestive of an inhibition of glutamate release. Presynaptic voltage-clamp experiments revealed a reversible reduction of Ca2+ currents by DHPG, with no significant modification of the presynaptic action potential waveform. Likewise, in approximately 50% of the tested cells, the CB1 receptor agonist (R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone (WIN) reversibly inhibited EPSCs, presynaptic Ca2+ currents, and exocytosis. For a given cell, the amount of inhibition by DHPG correlated with that by WIN. Moreover, the inhibitory action of DHPG was blocked by the CB1R antagonist N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM251) and occluded by WIN, indicating that DHPG and WIN operate via a common pathway. The inhibition of EPSCs by DHPG, but not by WIN, was abolished after dialyzing 40 mm BAPTA into the postsynaptic cell, suggesting that DHPG activated postsynaptic mGluRs. Light and electron microscopy immunolabeling indicated a presynaptic expression of CB1Rs and postsynaptic localization of mGluR1a. Our data suggest that activation of postsynaptic mGluRs triggers the Ca2+-dependent release of endocannabinoids that activate CB1 receptors on the calyx terminal, which leads to a reduction of presynaptic Ca2+ current and glutamate release.

Good players left on the sidelines: why some synaptic vesicles don't get in the game.

A key question in synaptic physiology is what determines the release probability of a synaptic vesicle. In this issue of Neuron, Wadel et al. shed UV light on this problem, finding that hard-to-release vesicles are too far from Ca2+ channels.

Long-term potentiation of glutamatergic synaptic transmission induced by activation of presynaptic P2Y receptors in the rat medial habenula nucleus.

A novel form of long-term potentiation of glutamatergic synaptic transmission is described in the rat medial habenula nucleus. It occurs when uridine 5'-triphosphate is bath applied at low micromolar concentrations and is prevented by Reactive Blue 2, suggesting that it is mediated by P2Y4 receptors. Uridine 5'-diphosphate can also cause such a Reactive Blue 2-sensitive potentiation, but at higher concentrations (200 microm), suggesting that this might also be an effect on the relatively uridine 5'-diphosphate-insensitive P2Y4 receptor. The potentiation is due to an increase in presynaptic release probability. It requires neither depolarization nor calcium influx postsynaptically and is thus probably non-Hebbian. When potentiation due to low concentrations of uridine 5'-triphosphate is inhibited in the presence of Reactive Blue 2, uridine 5'-triphosphate causes instead a significant inhibition of glutamate release. We suggest that this inhibition may be mediated by a Reactive Blue 2-insensitive P2Y2-like receptor. At higher concentrations of uridine 5'-triphosphate (200 micro m), the inhibitory effect dominates such that even in the absence of Reactive Blue 2 no potentiation is seen.