A comparative review on neuroethical issues in neuroscientific and neuroethical journals.

This study is a pilot literature review that compares the interest of neuroethicists and neuroscientists. It aims to determine whether there is a significant gap between the neuroethical issues addressed in philosophical neuroethics journals and neuroscience journals. We retrieved 614 articles from two specialist neuroethics journals ( and ) and 82 neuroethics-focused articles from three specialist neuroscience journals (, , and ).

Bright, non-blinking, and less-cytotoxic SiO2 beads with multiple CdSe/ZnS nanocrystals.

A method including surface silanization, phase transfer and self-assembly, and SiO2 shell growth has been developed to incorporate multiple hydrophobic CdSe/ZnS nanocrystals into SiO2 beads where they are well suited for bio-application due to their high brightness, less-cytotoxic, and non-blinking nature.

Technical note: a tool for determining rotational tilt axis with or without fiducial markers.

Virtually all reliable TEM tomographic reconstructions in life science depend upon cross-correlating successive images in a tilt-stack, and then using gold nanobeads as fiducial markers for determining the relative image rotation axis. Although the rotational tilt angle is one of the essential parameters affecting the quality of tomographic reconstructions, little is discussed about its determination. We provide here a simple tool based on the property of Fast Fourier Transformation for determining this rotation axis offset angle.

Resynchronization in neuronal network divided by femtosecond laser processing.

We demonstrated scission of a living neuronal network on multielectrode arrays (MEAs) using a focused femtosecond laser and evaluated the resynchronization of spontaneous electrical activity within the network. By an irradiation of femtosecond laser into hippocampal neurons cultured on a multielectrode array dish, neurites were cut at the focal point. After the irradiation, synchronization of neuronal activity within the network drastically decreased over the divided area, indicating diminished functional connections between neurons.

17beta-estradiol protects cortical neurons against oxidative stress-induced cell death through reduction in the activity of mitogen-activated protein kinase and in the accumulation of intracellular calcium.

Although many studies have suggested that estrogen acts as a neuroprotective agent in oxidative stress, the underlying mechanism has not been fully elucidated. In the present study, we examined the effect of 17beta-estradiol (17beta-E2) on H(2)O(2)-induced death signaling in cultured cortical neurons. Exposure of the cortical neurons to H(2)O(2) triggered a series of events, including overactivation of p44/42 MAPK and intracellular Ca(2+) accumulation via voltage-gated Ca(2+) channels and ionotropic glutamate receptors, resulting in apoptotic-like cell death.

Impact of the DISC1 Ser704Cys polymorphism on risk for major depression, brain morphology and ERK signaling.

Disrupted-in-schizophrenia 1 (DISC1), identified in a pedigree with a familial psychosis with the chromosome translocation (1:11), is a putative susceptibility gene for psychoses such as schizophrenia and bipolar disorder. Although there are a number of patients with major depressive disorder (MDD) in the family members with the chromosome translocation, the possible association with MDD has not yet been studied. We therefore performed an association study of the DISC1 gene with MDD and schizophrenia.

Phospholipid vesicle fusion on micropatterned polymeric bilayer substrates.

As an approach to create versatile model systems of the biological membrane we have recently developed a novel micropatterning strategy of substrate-supported planar lipid bilayers (SPBs) based on photolithographic polymerization of a diacetylene phospholipid, 1,2-bis(10,12-tricosadiynoyl)-sn-glycero-3-phosphocholine. The micropatterned SPBs are composed of a polymeric bilayer matrix and embedded fluid lipid bilayers. In this study, we investigated the incorporation of fluid bilayers into micropatterned polymeric bilayer matrices through the adsorption and reorganization of phospholipid vesicles (vesicle fusion).

Vitamin E protected cultured cortical neurons from oxidative stress-induced cell death through the activation of mitogen-activated protein kinase and phosphatidylinositol 3-kinase.

The role of vitamin E in the CNS has not been fully elucidated. In the present study, we found that pre-treatment with vitamin E analogs including alphaT (alpha-tocopherol), alphaT3 (alpha -tocotrienol), gammaT, and gammaT3 for 24 h prevented the cultured cortical neurons from cell death in oxidative stress stimulated by H2O2, while Trolox, a cell-permeable analog of alphaT, did not. The preventive effect of alphaT was dependent on de novo protein synthesis.

Development of new screening system for Alzheimer disease, in vitro Abeta sink assay, to identify the dissociation of soluble Abeta from fibrils.

Abeta is one of the primary therapeutic targets for Alzheimer disease (AD). Abeta vaccination induces the disappearance of Abeta deposits. Since few reports have focused on the reverse phase of Abeta aggregation, we established a new screening system, the in vitro Abeta sink assay, to clarify the process of dissociation of soluble forms from fibrils.

Brain-derived neurotrophic factor-induced potentiation of glutamate and GABA release: different dependency on signaling pathways and neuronal activity.

The mechanisms underlying BDNF-modulated neurotransmitter release remain elusive. Here, we found that 24-h exposure of postnatal cortical neurons to BDNF potentiated depolarization-evoked glutamate and GABA release in a protein synthesis-dependent manner. BDNF-potentiated glutamate release occurred through the PLC-gamma and MAPK pathways.

Subcellular localization of PMES-2 proteins regulated by their two cytoskeleton-associated domains.

1. PMES-2 is a protein, of which mRNA is translocated to the neurites of hippocampal neurons. Since the protein is present in the postsynaptic density, contributions to synaptic function have been predicted.

Long-term effects of muscle-derived protein with molecular mass of 77 kDa (MDP77) on nerve regeneration.

The long-term effects of the 77-kDa muscle-derived protein (MDP77) on motor and sensory nerve regeneration were examined in vivo. Fourteen-millimeter bridge grafts of the right sciatic nerve of SD rats were carried out with silicone tubes containing a solution of type I collagen together with 0, 5, 10, or 20 microg/ml recombinant human MDP77 (N = 10 in each group). Recovery of motor and sensory function was evaluated monthly by the maximal toe-spread index (TSI) and hot-plate test, respectively, for 6 months after the operation.

Diminished neuronal activity increases neuron-neuron connectivity underlying silent synapse formation and the rapid conversion of silent to functional synapses.

Neuronal activity regulates the synaptic strength of neuronal networks. However, it is still unclear how diminished activity changes connection patterns in neuronal circuits. To address this issue, we analyzed neuronal connectivity and relevant mechanisms using hippocampal cultures in which developmental synaptogenesis had occurred.

Trafficking of a ligand-receptor complex on the growth cones as an essential step for the uptake of nerve growth factor at the distal end of the axon: a single-molecule analysis.

The behavior of single molecules of neurotrophins on growth cones was observed by the use of the fluorescent conjugate of nerve growth factor (NGF), Cy3-NGF. After the application of 0.4 nm Cy3-NGF, chick dorsal root ganglion growth cones responded within 1 min of adding the stimulus by expanding their lamellipodia.

Neurocrescin is specifically cleaved after the sequence DESD in a caspase-3-independent manner.

1. A neurite outgrowth factor, neurocrescin (NC), which we previously identified from an extract of denervated skeletal muscle, was endoproteolytically processed in cell transfectants. In addition to the processing site identified in NC (DESD358/F) being similar to the optimal recognition sequence of group II caspases, DExD, cleavage site mutations confirmed the involvement of caspase(s) in NC processing.

GroEL chaperone binding to beetle luciferases and the implications for refolding when co-expressed.

The folding of many proteins including luciferase in vivo requires the assistance of molecular chaperone proteins. To understand how a chaperone targets luciferase, we took three luciferases that give different bioluminescence with the same luciferin substrate and with differences in homology. The three luciferase genes, firefly luciferase (FF-Luc) (from Pyrocoelia miyako), and red (RE-Luc) and green (GR-Luc) bioluminescence-emitting luciferases (from Phrixothrix railroad-worms), were expressed in Escherichia coli to produce fusion proteins with predicted molecular masses.

Evidence of novel neuronal functions of dysbindin, a susceptibility gene for schizophrenia.

Genetic variation in dysbindin (DTNBP1: dystrobrevin-binding protein 1) has recently been shown to be associated with schizophrenia. The dysbindin gene is located at chromosome 6p22.3, one of the most promising susceptibility loci in schizophrenia linkage studies.

Micropatterned composite membranes of polymerized and fluid lipid bilayers.

Micropatterned composite membranes of polymerized and fluid lipid bilayers were constructed on solid substrates. Lithographic photopolymerization of a diacetylene-containing phospholipid, 1,2-bis(10,12-tricosadiynoyl)-sn-glycero-3-phosphocholine (DiynePC), and subsequent removal of nonreacted monomers by a detergent solution (0.1 M sodium dodecyl sulfate (SDS)) yielded a patterned polymeric bilayer matrix on the substrate.

Neuronal roles of the integrin-associated protein (IAP/CD47) in developing cortical neurons.

Little is known about the role of the integrin-associated protein (IAP, or CD47) in neuronal development and its function in the central nervous system. We investigated neuronal responses in IAP-overexpressing cortical neurons using a virus-gene transfer system. We found that dendritic outgrowth was significantly enhanced in IAP (form 4)-transfected neurons.

Muscle-specific protein MDP77 specifically promotes motor nerve regeneration in rats.

This study has examined the effects of recombinant human MDP77 (rhMDP77) on sciatic motor nerve regeneration in vivo. We carried out bridge grafting (14 mm) into the sciatic nerve of Sprague-Dawley rats using silicone tubes containing a mixture of type-I collagen and 0, 5, 10, or 20 microg/ml of rhMDP77, or containing phosphate-buffered solution (N = 6 in each group). Electrophysiological and histological evaluations carried out 12 weeks after implantation suggest that rhMDP77 has a positive effect on terminal and collateral sprouting of regenerating nerves and thereby promotes motor nerve regeneration in a dose-dependent manner.

Highly oriented aragonite nanocrystal-biopolymer composites in an aragonite brick of the nacreous layer of Pinctada fucata.

13C CP/MAS NMR and FE/TEM measurements of the aragonite brick of the nacreous layer of Pinctada fucata indicate that it assembles with highly oriented aragonite nanocrystals, which are regulated by biopolymers.

Re-expression of NR2B-containing NMDA receptors in vitro by suppression of neuronal activity.

N-methyl-D-aspartate receptors (NMDARs) are known to play critical roles in the development of the nervous system, and their expression is regulated in an activity-dependent fashion during development. However, the regulation of NMDAR expression after circuit formation is less well understood. To examine this, we performed patch-clamp recordings from chick cerebral neurons in an activity-controlled culture.

Nerve growth factor-induced glutamate release is via p75 receptor, ceramide, and Ca(2+) from ryanodine receptor in developing cerebellar neurons.

Very little is known about the contribution of a low affinity neurotrophin receptor, p75, to neurotransmitter release. Here we show that nerve growth factor (NGF) induced a rapid release of glutamate and an increase of Ca2+ in cerebellar neurons through a p75-dependent pathway. The NGF-induced release occurred even in the presence of the Trk inhibitor K252a.

Estrogen enhances depolarization-induced glutamate release through activation of phosphatidylinositol 3-kinase and mitogen-activated protein kinase in cultured hippocampal neurons.

Changes in synaptic efficacy are considered necessary for learning and memory. Recently, it has been suggested that estrogen controls synaptic function in the central nervous system. However, it is unclear how estrogen regulates synaptic function in central nervous system neurons.

Cloning and characterization of a novel synaptosome-enriched mRNA that encodes 31 kDa protein.

Although a subpopulation of mRNAs has been identified as translocated to the dendrites or the synaptic regions of neurons, the translocational mechanism has not been elucidated. To find mRNAs enriched in synapses, we compared the synaptosomal mRNAs with those from whole forebrain using differential display (DD). We cloned one of these mRNAs, which encoded a novel 31 kDa protein (PMES-2).