Synthesis, Electrochemistry, and Excited-State Properties of Three Ru(II) Quaterpyridine Complexes

The complexes [Ru(qpy)LL′]2+ (qpy = 2,2′:6′,2″:6″,2‴-quaterpyridine), with 1: L = acetonitrile, L′= chloride; 2: L = L′= acetonitrile; and 3: L = L′= vinylpyridine, have been prepared from [Ru(qpy) (Cl)2]. Their absorption spectra in CH3CN exhibit broad metal-to-ligand charge transfer (MLCT) absorptions arising from overlapping 1A1 → 1MLCT transitions. Photoluminescence is not observed at room temperature, but all three are weakly emissive in 4:1 ethanol/methanol glasses at 77 K with broad, featureless emissions observed between 600 and 1000 nm consistent with MLCT phosphorescence. Cyclic voltammograms in CH3CN reveal the expected RuIII/II redox couples. In 0.1 M trifluoroacetic acid (TFA), 1 and 2 undergo aquation to give [RuII(qpy)(OH2)2]2+, as evidenced by the appearance of waves for the couples [RuIII(qpy)(OH2)2]3+/[RuII(qpy)(OH2)2]2+, [RuIV(qpy)(O)(OH2)]2+/[RuIII(qpy)(OH2)2]3+, and [RuVI(qpy)(O)2]2+/[RuIV(qpy)(O)(OH2)]2+ in cyclic voltammograms

Dye-Sensitized Nonstoichiometric Strontium Titanate Core-Shell Photocathodes for Photoelectrosynthesis Applications

A core-shell approach that utilizes a high-surface-area conducting core and an outer semiconductor shell is exploited here to prepare p-type dye-sensitized solar energy cells that operate with a minimal applied bias. Photocathodes were prepared by coating thin films of nanocrystalline indium tin oxide with a 0.8 nm Al2O3 seeding layer, followed by the chemical growth of nonstoichiometric strontium titanate. Films were annealed and sensitized with either a porphyrin chromophore or a chromophore-catalyst molecular assembly consisting of the porphyrin covalently tethered to the ruthenium complex. The sensitized photoelectrodes produced cathodic photocurrents of up to -315 μA/cm2 under simulated sunlight (AM1.5G, 100 mW/cm2) in aqueous media, pH 5. The photocurrent was increased by the addition of regenerative hole donors to the system, consistent with slow interfacial recombination kinetics, an important property of p-type dye-sensitized electrodes

Synthesis, characterization, and water oxidation by a molecular chromophore-catalyst assembly prepared by atomic layer deposition. The “mummy” strategy

A Ru( ii )-polypyridyl chromophore-catalyst assembly for light-assisted water oxidation is constructed using atomic layer deposition with no covalent bonds between molecules required for bilayer formation

Developmental regulation of neural cell adhesion molecule in human prefrontal cortex

Neural cell adhesion molecule (NCAM) is a membrane-bound cell recognition molecule that exerts important functions in normal neurodevelopment including cell migration, neurite outgrowth, axon fasciculation, and synaptic plasticity. Alternative splicing of NCAM mRNA generates three main protein isoforms: NCAM-180, -140, and -120. Ectodomain shedding of NCAM isoforms can produce an extracellular 105–115 kDa soluble NCAM fragment (NCAM-EC) and a smaller intracellular cytoplasmic fragment (NCAM-IC). NCAM also undergoes a unique post-translational modification in brain by the addition of polysialic acid (PSA)-NCAM. Interestingly, both PSA-NCAM and NCAM-EC have been implicated in the pathophysiology of schizophrenia. The developmental expression patterns of the main NCAM isoforms and PSA-NCAM have been described in rodent brain, but no studies have examined NCAM expression across human cortical development. Western blotting was used to quantify NCAM in human postmortem prefrontal cortex in 42 individuals ranging in age from mid-gestation to early adulthood. Each NCAM isoform (NCAM-180, -140, and -120), post-translational modification (PSA-NCAM) and cleavage fragment (NCAM-EC and NCAM-IC) demonstrated developmental regulation in frontal cortex. NCAM-180, -140, and -120, as well as PSA-NCAM, and NCAM-IC all showed strong developmental regulation during fetal and early postnatal ages, consistent with their identified roles in axon growth and plasticity. NCAM-EC demonstrated a more gradual increase from the early postnatal period to reach a plateau by early adolescence, potentially implicating involvement in later developmental processes. In summary, this study implicates the major NCAM isoforms, PSA- NCAM and proteolytically cleaved NCAM in pre- and postnatal development of the human prefrontal cortex. These data provide new insights on human cortical development and also provide a basis for how altered NCAM signaling during specific developmental intervals could affect synaptic connectivity and circuit formation, and thereby contribute to neurodevelopmental disorders

Neural Cell Adhesion Molecule NrCAM Regulates Semaphorin 3F-Induced Dendritic Spine Remodeling

Neuron-glial related cell adhesion molecule (NrCAM) is a regulator of axon growth and repellent guidance, and has been implicated in autism spectrum disorders. Here a novel postsynaptic role for NrCAM in Semaphorin3F (Sema3F)-induced dendritic spine remodeling was identified in pyramidal neurons of the primary visual cortex (V1). NrCAM localized to dendritic spines of star pyramidal cells in postnatal V1, where it was coexpressed with Sema3F. NrCAM deletion in mice resulted in elevated spine densities on apical dendrites of star pyramidal cells at both postnatal and adult stages, and electron microscopy revealed increased numbers of asymmetric synapses in layer 4 of V1. Whole-cell recordings in cortical slices from NrCAM-null mice revealed increased frequency of mEPSCs in star pyramidal neurons. Recombinant Sema3F-Fc protein induced spine retraction on apical dendrites of wild-type, but not NrCAM-null cortical neurons in culture, while re-expression of NrCAM rescued the spine retraction response. NrCAM formed a complex in brain with Sema3F receptor subunits Neuropilin-2 (Npn-2) and PlexinA3 (PlexA3) through an Npn-2-binding sequence (TARNER) in the extracellular Ig1 domain. A trans heterozygous genetic interaction test demonstrated that Sema3F and NrCAM pathways interacted in vivo to regulate spine density in star pyramidal neurons. These findings reveal NrCAM as a novel postnatal regulator of dendritic spine density in cortical pyramidal neurons, and an integral component of the Sema3F receptor complex. The results implicate NrCAM as a contributor to excitatory/inhibitory balance in neocortical circuits

Solar water splitting in a molecular photoelectrochemical cell

Solar water splitting into H2 and O2 with visible light has been achieved by a molecular assembly. The dye sensitized photoelectrosynthesis cell configuration combined with core–shell structures with a thin layer of TiO2 on transparent, nanostructured transparent conducting oxides (TCO), with the outer TiO2 shell formed by atomic layer deposition. In this configuration, excitation and injection occur rapidly and efficiently with the injected electrons collected by the nanostructured TCO on the nanosecond timescale where they are collected by the planar conductive electrode and transmitted to the cathode for H2 production. This allows multiple oxidative equivalents to accumulate at a remote catalyst where water oxidation catalysis occurs

NrCAM Deletion Causes Topographic Mistargeting of Thalamocortical Axons to the Visual Cortex and Disrupts Visual Acuity

NrCAM is a neural cell adhesion molecule of the L1 family that has been linked to autism spectrum disorders (ASDs), a disease spectrum in which abnormal thalamocortical connectivity may contribute to visual processing defects. Here we show that NrCAM interaction with Neuropilin-2 (Npn-2) is critical for Semaphorin3F (Sema3F)-induced guidance of thalamocortical axon subpopulations at the ventral telencephalon (VTe), an intermediate target for thalamic axon sorting. Genetic deletion of NrCAM or Npn-2 caused contingents of embryonic thalamic axons to misproject caudally in the VTe, away from a caudal-high Sema3F gradient. The resultant thalamocortical map of NrCAM null mutants showed striking mistargeting of motor and somatosensory thalamic axon contingents to the primary visual cortex, but retino-geniculate targeting and segregation were normal. NrCAM formed a molecular complex with Npn-2 in brain and neural cells, and was required for Sema3F-induced growth cone collapse in thalamic neuron cultures, consistent with a vital function for NrCAM in Sema3F-induced axon repulsion. NrCAM null mice displayed reduced responses to visual evoked potentials (VEPs) recorded from layer IV in the binocular zone of primary visual cortex (V1), particularly when evoked from the ipsilateral eye, indicating abnormal visual acuity and ocularity. These results demonstrate that NrCAM is required for normal maturation of cortical visual acuity, and suggest that the aberrant projection of thalamic motor and somatosensory axons to the visual cortex in NrCAM null mutant mice impairs cortical functions

Controlling ground and excited state properties through ligand changes in ruthenium polypyridyl complexes

The capture and storage of solar energy requires chromophores that absorb light throughout the solar spectrum. We report here the synthesis, characterization, electrochemical, and photophysical properties of a series of Ru(II) polypyridyl complexes of the type [Ru(bpy)2(N–N)]2+ (bpy = 2,2'-bipyridine; N–N is a bidentate polypyridyl ligand). In this series, the nature of the N–N ligand was altered, either through increased conjugation or incorporation of noncoordinating heteroatoms, as a way to use ligand electronic properties to tune redox potentials, absorption spectra, emission spectra, and excited state energies and lifetimes. Electrochemical measurements show that lowering the π* orbitals on the N–N ligand results in more positive Ru3+/2+ redox potentials and more positive first ligand-based reduction potentials. The metal-to-ligand charge transfer absorptions of all of the new complexes are mostly red-shifted compared to Ru(bpy)32+ (λmax = 449 nm) with the lowest energy MLCT absorption appearing at λmax = 564 nm. Emission energies decrease from λmax = 650 nm to 885 nm across the series. One-mode Franck–Condon analysis of room-temperature emission spectra are used to calculate key excited state properties, including excited state redox potentials. The impacts of ligand changes on visible light absorption, excited state reduction potentials, and Ru3+/2+ potentials are assessed in the context of preparing low energy light absorbers for application in dye-sensitized photoelectrosynthesis cells