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  • COA 100980

    Document Type:
    Certificate of Analysis
    Product Catalog Number:
    100980

  • Expression pattern of NOGO-A protein in the human nervous system. 15616791

    The distribution pattern of NOGO-A protein, an important axon growth inhibitory molecule and member of the reticulon family, has been investigated in the adult human brain, spinal cord, retina and dorsal root ganglia. Intense NOGO-A immunoreactivity was detected in oligodendroglial cell bodies and their myelin sheaths in nerve fibre tracts of the central nervous system. Furthermore, numerous populations of neurons in the brain and spinal cord expressed NOGO-A to a variable extent in their cell bodies and neurites, suggesting additional, as-yet-unknown, functions of this protein.
    Document Type:
    Reference
    Product Catalog Number:
    AB980

  • Remyelination of cytokine- or antibody-demyelinated CNS aggregate cultures is inhibited by macrophage supplementation. 14730701

    Remyelination in CNS aggregate cultures is determined both by macrophage enrichment and the mode of demyelination. Despite the same degree of myelin loss, accumulation of MBP in anti-MOG antibody-demyelinated aggregates overtakes that of controls, while recovery is significantly delayed following IFN-gamma-induced demyelination. In antibody-treated cultures, remyelination was associated with a significant increase in culture supernatant levels of TGF-beta1, FGF-2, and PDGF-AA as well as an induction of TNF-alpha immediately following removal of the demyelinating insult. The impaired recovery in IFN-gamma-treated cultures, denoted by a significant reduction in TGF-beta1, was reversed by treatment with hrTGF-beta1. Macrophage supplementation of the cultures prior to the addition of either demyelinating agent induced a greater degree of myelin loss followed by incomplete remyelination in both cases. This failure to remyelinate was associated in both groups with a several-fold elevation in TNF-alpha and with modest increases in PDGF-AA and FGF-2 in the antibody-treated cultures. In contrast, macrophage supplementation to mature cultures in the absence of any demyelinating treatment resulted in enhanced accumulation of MBP associated with a promyelinative growth factor and TNF-alpha profile similar to that in aggregates enriched with macrophages at the outset of the culture period. Hence, effector elements of the adaptive immune response appear to override promyelinogenic in favor of proinflammatory macrophage factors in mature CNS aggregates, counteracting the potential for myelin repair.
    Document Type:
    Reference
    Product Catalog Number:
    AB980

  • Alsin/Rac1 signaling controls survival and growth of spinal motoneurons. 16802292

    OBJECTIVE: Recessive mutations in alsin, a guanine-nucleotide exchange factor for the GTPases Rab5 and Rac1, cause juvenile amyotrophic lateral sclerosis (ALS2) and related motoneuron disorders. Alsin function in motoneurons remained unclear because alsin knock-out mice do not develop overt signs of motoneuron degeneration. METHODS: To generate an alsin loss-of-function model in an ALS-relevant cell type, we developed a new small interfering RNA electroporation technique that allows efficient knock down of alsin in embryonic rat spinal motoneurons. RESULTS: After small interfering RNA-mediated alsin knockdown, cultured motoneurons displayed a reduced apparent size of EEA1-labeled early endosomes and an increased intracellular accumulation of transferrin and L1CAM. Alsin knockdown induced cell death in 32 to 48% of motoneurons and significantly inhibited axon growth in the surviving neurons. Both cellular phenotypes were mimicked by expression of a dominant-negative Rac1 mutant and were completely blocked by expression of a constitutively active Rac1 mutant. Expression of dominant-negative or constitutively active forms of Rab5 had no such effects. INTERPRETATION: Our data demonstrate that alsin controls the growth and survival of motoneurons in a Rac1-dependant manner. The strategy reported here illustrates how small interfering RNA electroporation can be used to generate cellular models of neurodegenerative disease involving a loss-of-function mechanism.
    Document Type:
    Reference
    Product Catalog Number:
    AB1987
    Product Catalog Name:
    Anti-Neurofilament M (145 kDa) Antibody, CT

  • Neurotransmitters in airway parasympathetic neurons altered by neurotrophin-3 and repeated allergen challenge. 19901346

    Changes in airway nerves associated with chronic inflammation may underlie the pathogenesis and symptoms of lower airway diseases, such as asthma. The molecules most likely causing such alterations are neurotrophins (NTs) and/or related neurokines. In several species, including humans, lower airway parasympathetic postganglionic neurons that project axons to airway smooth muscle are either cholinergic or nonadrenergic noncholinergic (NANC), the latter synthesizing vasoactive intestinal peptide and nitric oxide, but not acetylcholine. In guinea pig trachealis smooth muscle, cholinergic nerve terminals arise from ganglionic neurons located near the tracheal smooth muscle, whereas the source of NANC nerve fibers is from neurons in ganglia located in the adjacent myenteric plexus of the esophagus, making this an ideal species to study regulation of parasympathetic neurotransmitter phenotypes. In the present study, we determined that, 48 hours after repeated allergen challenge, the NANC phenotype of airway parasympathetic ganglionic neurons changed to a cholinergic phenotype, and NT-3 mimicked this change. Nerve growth factor, brain-derived neurotrophic factor, leukemia inhibitory factor, or IL-1β had no effect on either phenotype, and they did not induce these neurons to synthesize substance P or tyrosine hydroxylase. These results indicate a role for inflammation and NT-3 in regulating biochemical and anatomical characteristics of principal neurons in adult airway parasympathetic ganglia.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Involvement of endoplasmic reticulum stress in optic nerve degeneration following N-methyl-D-aspartate-induced retinal damage in mice. 22674348

    We evaluated time-dependent optic nerve degeneration and the role of endoplasmic reticulum (ER) stress in this process following retinal ganglion cell death in mice. Retinal damage was induced by intravitreal injection of N-methyl-D-aspartate (NMDA). Neurofilament heavy (NFH)- and phosphorylated NFH (pNFH)-positive axons were time-dependently decreased in optic nerves at 1, 3, 7, 14, and 28 days after NMDA injection. Expression of glial fibrillary acidic protein (GFAP)-positive astroglial cells and ionized calcium-binding adaptor molecule 1 (Iba1)-positive microglial cells showed a significant increase in the optic nerve at 7, 14, and 28 days after NMDA injection. In contrast, expression of myelin basic protein (MBP)-positive oligodendrocytes showed a significant decrease in the optic nerve at 7, 14, and 28 days after NMDA injection. In quantitative RT-PCR analysis, expressions of glucose-regulated protein 78 (Grp78)/BiP, Grp94, Calreticulin, C/EBP homologous protein (Chop), and the ER degradation enhancer mannosidase alpha-like 1 (Edem1) genes were increased in the optic nerve at 14 days after NMDA injection. In addition, the Grp94 gene was increased at 7 days after NMDA injection, and the Edem1 gene was increased at 3, 7, and 28 days after NMDA injection. GRP78 and CHOP proteins were colocalized with MBP in the optic nerve after NMDA injection. These findings suggest that the axonal degeneration is dramatic until 7 days after NMDA injection and that glial cells may play some role in the degeneration of the optic nerve. Furthermore, ER stress may play a pivotal role in the decrease of MBP-positive oligodendrocytes after NMDA-induced retinal damage. © 2012 Wiley Periodicals, Inc.
    Document Type:
    Reference
    Product Catalog Number:
    AB1989
    Product Catalog Name:
    Anti-Neurofilament H (200 kDa) Antibody, CT

  • Coxsackievirus preferentially replicates and induces cytopathic effects in undifferentiated neural progenitor cells. 21471247

    Enteroviruses, including coxsackieviruses, exhibit significant tropism for the central nervous system, and these viruses are commonly associated with viral meningitis and encephalitis. Previously, we described the ability of coxsackievirus B3 (CVB3) to infect proliferating neuronal progenitor cells located in the neonatal subventricular zone and persist in the adult murine central nervous system (CNS). Here, we demonstrate that cultured murine neurospheres, which comprise neural stem cells and their progeny at different stages of development, were highly susceptible to CVB3 infection. Neurospheres, or neural progenitor and stem cells (NPSCs), isolated from neonatal C57BL/6 mice, supported high levels of infectious virus production and high viral protein expression levels following infection with a recombinant CVB3 expressing enhanced green fluorescent protein (eGFP) protein. Similarly, NPSCs isolated from neonatal actin-promoter-GFP transgenic mice (actin-GFP NPSCs) were highly susceptible to infection with a recombinant CVB3 expressing DsRed (Discosoma sp. red fluorescent protein). Both nestin-positive and NG2(+) progenitor cells within neurospheres were shown to preferentially express high levels of viral protein as soon as 24 h postinfection (p.i.). By day 3 p.i., viral protein expression and viral titers increased dramatically in NPSCs with resultant cytopathic effects (CPE) and eventual cell death. In contrast, reduced viral replication, lower levels of CPE, and diminished viral protein expression levels were observed in NPSCs differentiated for 5 or 16 days in the presence of fetal bovine serum (FBS). Despite the presence of CPE and high levels of cell death following early CVB3 infection, surviving neurospheres were readily observed and continued to express detectable levels of viral protein as long as 37 days after initial infection. Also, CVB3 infection of actin-GFP NPSCs increased the percentage of cells expressing neuronal class III β-tubulin following their differentiation in the presence of FBS. These results suggest that neural stem cells may be preferentially targeted by CVB3 and that neurogenic regions of the CNS may support persistent viral replication in the surviving host. In addition, normal progenitor cell differentiation may be altered in the host following infection.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • The spinal precerebellar nuclei: calcium binding proteins and gene expression profile in the mouse. 22579822

    We have localized the spinocerebellar neuron groups in C57BL/6J mice by injecting the retrograde neuronal tracer Fluoro-Gold into the cerebellum and examined the distribution of SMI 32 and the calcium-binding proteins (CBPs), calbindin-D-28K (Cb), calretinin (Cr), and parvalbumin (Pv) in the spinal precerebellar nuclei. The spinal precerebellar neuron clusters identified were the dorsal nucleus, central cervical nucleus, lumbar border precerebellar nucleus, lumbar precerebellar nucleus, and sacral precerebellar nucleus. Some dispersed neurons in the deep dorsal horn and spinal laminae 6-8 also projected to the cerebellum. Cb, Cr, Pv, and SMI 32 were present in all major spinal precerebellar nuclei and Pv was the most commonly observed CBP. A number of genes expressed in hindbrain precerebellar nuclei are also expressed in spinal precerebellar groups, but there were some differences in gene expression profile between the different spinal precerebellar nuclei, pointing to functional diversity amongst them.
    Document Type:
    Reference
    Product Catalog Number:
    AB5054