We demonstrate vertically aligned epitaxial GaAs nanowires of excellent crystallographic quality and optimal shape, grown by Au nanoparticle-catalyzed metalorganic chemical vapor deposition. This is achieved by a two-temperature growth procedure, consisting of a brief initial high-temperature growth step followed by prolonged growth at a lower temperature. The initial high-temperature step is essential for obtaining straight, vertically aligned epitaxial nanowires on the (111)B GaAs substrate. The lower temperature employed for subsequent growth imparts superior nanowire morphology and crystallographic quality by minimizing radial growth and eliminating twinning defects. Photoluminescence measurements confirm the excellent optical quality of these two-temperature grown nanowires. Two mechanisms are proposed to explain the success of this two-temperature growth process, one involving Au nanoparticle-GaAs interface conditions and the other involving melting-solidification temperature hysteresis of the Au-Ga nanoparticle alloy.

The neurobiological underpinnings of mood and anxiety disorders have been linked to the nucleus accumbens (NAc), a region important in processing the rewarding and emotional salience of stimuli. Using chronic social defeat stress, an animal model of mood and anxiety disorders, we investigated whether alterations in synaptic plasticity are responsible for the long-lasting behavioral symptoms induced by this form of stress. We hypothesized that chronic social defeat stress alters synaptic strength or connectivity of medium spiny neurons (MSNs) in the NAc to induce social avoidance. To test this, we analyzed the synaptic profile of MSNs via confocal imaging of Lucifer-yellow-filled cells, ultrastructural analysis of the postsynaptic density, and electrophysiological recordings of miniature EPSCs (mEPSCs) in mice after social defeat. We found that NAc MSNs have more stubby spine structures with smaller postsynaptic densities and an increase in the frequency of mEPSCs after social defeat. In parallel to these structural changes, we observed significant increases in IκB kinase (IKK) in the NAc after social defeat, a molecular pathway that has been shown to regulate neuronal morphology. Indeed, we find using viral-mediated gene transfer of dominant-negative and constitutively active IKK mutants that activation of IKK signaling pathways during social defeat is both necessary and sufficient to induce synaptic alterations and behavioral effects of the stress. These studies establish a causal role for IKK in regulating stress-induced adaptive plasticity and may present a novel target for drug development in the treatment of mood and anxiety disorders in humans.

We have synthesized ternary InGaAs nanowires on (111)B GaAs surfaces by metal-organic chemical vapor deposition. Au colloidal nanoparticles were employed to catalyze nanowire growth. We observed the strong influence of nanowire density on nanowire height, tapering, and base shape specific to the nanowires with high In composition. This dependency was attributed to the large difference of diffusion length on (111)B surfaces between In and Ga reaction species, with In being the more mobile species. Energy dispersive X-ray spectroscopy analysis together with high-resolution electron microscopy study of individual InGaAs nanowires shows large In/Ga compositional variation along the nanowire supporting the present diffusion model. Photoluminescence spectra exhibit a red shift with decreasing nanowire density due to the higher degree of In incorporation in more sparsely distributed InGaAs nanowires.

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SUMMARY p11, through unknown mechanisms, is required for behavioral and cellular responses to selective serotonin-reuptake inhibitors (SSRIs). Here we have identified SMARCA3, a chromatin-remodeling factor, as a novel target for the p11/annexin A2 heterotetrameric complex. Determination of the crystal structure indicates that SMARCA3 peptide binds to a hydrophobic pocket in the heterotetramer. Formation of this complex increases the DNA binding affinity of SMARCA3 and its localization to the nuclear matrix fraction. In the dentate gyrus, both p11 and SMARCA3 are highly enriched in hilar mossy cells and basket cells. In response to the SSRI, fluoxetine, the expression of p11 is induced in both cell types, and the amount of the ternary complex of p11/annexin A2/SMARCA3 is increased. SSRI-induced neurogenesis and behavioral responses are abolished by constitutive knockout of SMARCA3. Our studies indicate a central role for a chromatin-remodeling factor in the SSRI/p11 signaling pathway, and suggest a novel approach to the development of improved antidepressant therapies.

Large energy shifts in the luminescence emission from strained InGaAs quantum dots are observed as a result of postgrowth annealing and also when raising the upper cladding layer growth temperatures. These blueshifts occur concurrently with narrowing (from 61 to 24 meV) of the full width at half-maxima for the emission from the quantum dot ensemble. These energy shifts can be explained by interdiffusion or intermixing of the interfaces rather than strain effects due to variations in capping layer thickness. Temperature behavior of the luminescence in annealed and nonannealed samples indicates a change in the shape and depth of the quantum dot confining potential. Quenching of the wetting layer luminescence after interdiffusion is also observed.

Synaptojanin 1 is a polyphosphoinositide phosphatase concentrated in presynaptic nerve terminals, where it dephosphorylates a pool of phosphatidylinositol 4,5-bisphosphate implicated in synaptic vesicle recycling. Like other proteins with a role in endocytosis, synaptojanin 1 undergoes constitutive phosphorylation in resting synapses and stimulation-dependent dephosphorylation by calcineurin. Here, we show that cyclin-dependent kinase 5 (Cdk5) phosphorylates synaptojanin 1 and regulates its function both in vitro and in intact synaptosomes. Cdk5 phosphorylation inhibited the inositol 5-phosphatase activity of synaptojanin 1, whereas dephosphorylation by calcineurin stimulated such activity. The activity of synaptojanin 1 was also stimulated by its interaction with endophilin 1, its major binding partner at the synapse. Notably, Cdk5 phosphorylated serine 1144, which is adjacent to the endophilin binding site. Mutation of serine 1144 to aspartic acid to mimic phosphorylation by Cdk5 inhibited the interaction of synaptojanin 1 with endophilin 1. These results suggest that Cdk5 and calcineurin may have an antagonistic role in the regulation of synaptojanin 1 recruitment and activity, and therefore in the regulation of phosphatidylinositol 4,5-bisphosphate turnover at synapses. P hosphoinositides are key regulators of cell physiology. In particular, phosphatidylinositol (PI) 4,5-bisphosphate [PI(4,5)P 2 ] plays a major regulatory role at the cell surface, both as a precursor of important signaling molecules, as well as via interactions with cytosolic and membrane proteins (1-4). In nerve terminals, phospholipase C-mediated cleavage of PI(4,5)P 2 controls the efficiency of the depolarization-exocytosis coupling of synaptic vesicles via the actions of inositol 1,4,5-trisphosphate and diacylglycerol (DAG) on Ca 2ϩ signaling (5), and the additional action of DAG on Munc13 family proteins, key players in the ''priming'' of synaptic vesicle for exocytosis (6, 7). Furthermore, several proteins of the exocytic machinery, including the Ca 2ϩ sensor synaptotagmin, bind to and are regulated directly by PI(4,5)P 2 (8). Likewise, a variety of proteins implicated in synaptic vesicles endocytosis, such as the clathrin adaptor proteins AP2, AP180, and epsin, as well as the GTPase dynamin and other endocytic accessory factors, contain PI(4,5)P 2 binding sites (9-12). Binding of these proteins to PI(4,5)P 2 is thought to contribute to their recruitment to the plasma membrane and therefore to clathrin coat nucleation (13,14).Recent studies have implicated dephosphorylation of PI(4,5)P 2 by the polyphosphoinositide phosphatase synaptojanin 1, a pathway that does not produce inositol 1,4,5-trisphosphate and diacylglycerol, as an additional important regulatory mechanism at synapses (15)(16)(17)(18)(19)(20)(21)(22). This enzyme is concentrated in nerve terminals, where it is found in the cytosol, and also partially associated with endocytic intermediates (23, 24). The synaptojanin 1 molecule comprises two distinct inositol phosphatase do...