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  • 1
    Electronic Resource
    Electronic Resource
    Origin of Ischemia-Induced Glutamate Efflux in the CA1 Field of the Gerbil Hippocampus: An In Vivo Brain Microdialysis Study (1994)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 63 (1994), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: In vivo brain microdialysis experiments were performed in the gerbil to evaluate the origin of accumulation of extracellular glutamate under transient ischemia. Microdialysis probes were positioned in the CA1 field of the hippocampus in which proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals had been induced by 5-min ischemia 10–14 days before the microdialysis experiment; in the white matter of the cerebral cortex, which contained few neurons, few presynaptic terminals, and many astrocytes; or in the histologically normal CA1 field of the hippocampus, and then 5- or 20-min ischemia was induced. When 5-min ischemia was induced, no significant increase in glutamate content was observed in the CA1 field that showed proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals and in the white matter of the cerebral cortex, whereas a significant increase in glutamate (15-fold) was observed in the histologically normal CA1 field. When 20-min ischemia was induced, no significant increase in glutamate content was observed in the CA1 field that showed proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals and in the white matter during the first 10 min after the onset of 20-min ischemia, but remarkable ischemia-induced increases in glutamate were observed during the last 10 min of 20-min ischemia in both areas. An excessive increase in glutamate (100-fold) was observed during 20-min ischemia in the normal CA1 field of the hippocampus. When a probe was positioned in the CA1 field of the hippocampus in which presynaptic terminals of Schaffer collaterals and commissural fibers had been eliminated by bilateral kainate injections into the lateral ventricles 4–7 days before the microdialysis experiment and then 5-min ischemia was induced, a significant increase in glutamate was observed during the last half of 5-min ischemia. These results suggest that the efflux of glutamate from astrocytes does not contribute to the large ischemia-induced glutamate accumulation in the CA1 field of the hippocampus during 5-min ischemia but contributes to the ischemia-induced increase in glutamate level during ischemia with a longer duration and that ischemia-induced efflux of glutamate in the CA1 field during 5-min ischemia originates mainly from neuronal elements: presynaptic terminals and postsynaptic neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1994.63062152.x
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  • 2
    Electronic Resource
    Electronic Resource
    Prosaposin Facilitates Sciatic Nerve Regeneration In Vivo (1996)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 66 (1996), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Prosaposin, a multifunctional protein, is the precursor of saposins, which activate sphingolipid hydrolases. In addition to acting as a precursor for saposins, prosaposin has been shown to rescue hippocampal CA1 neurons from lethal ischemic damage in vivo and to promote neurite extension of neuroblastoma cells in vitro. Here we show that prosaposin, when added to a collagen-filled nerve guide after sciatic nerve transection in guinea pigs, increased dramatically the number of regenerating nerve fibers within the guide. To identify the target neurons of prosaposin during peripheral nerve regeneration, we determined the degree of atrophy and chromatolysis of neurons in the spinal anterior horn and dorsal root ganglia on the prosaposin-treated and untreated side. The effect of prosaposin on large spinal neurons and small neurons of the dorsal root ganglion was more conspicuous. Subsequent immunohistochemistry demonstrated that the atrophy of cholinergic large neurons in the anterior horn is prevented to significant extent by prosaposin treatment. These findings suggest that prosaposin promotes peripheral nerve regeneration by acting on α-motor neurons in the anterior horn and on small sensory neurons in the dorsal root ganglion. The present study raises the possibility of using prosaposin as a tool for the treatment of peripheral nerve injuries.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1996.66052019.x
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  • 3
    Electronic Resource
    Electronic Resource
    A Hydrophilic Peptide Comprising 18 Amino Acid Residues of the Prosaposin Sequence Has Neurotrophic Activity In Vitro and In Vivo (1996)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 66 (1996), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Prosaposin, a 517-amino-acid glycoprotein, not only acts as the precursor of saposin A, B, C, and D but also possesses neurotrophic activity to rescue hippocampal CA1 neurons from ischemic damage in vivo and to promote neurite extension of neuroblastoma cells in vitro. Recently, the trophic activity of prosaposin on human neuroblastoma cells has been shown to reside in the NH2-terminal hydrophilic sequence (LIDNNRTEEILY) of the human saposin C. Here we show that prosaposin, saposin C, and a peptide comprising the 18-amino-acid sequence (18-mer peptide; LSELIINNATEELLIKGL) located in the NH2-terminal hydrophilic sequence of the rat saposin C-domain promoted survival and neurite outgrowth of cultured rat hippocampal neurons in a dose-dependent manner. Moreover, infusion for 7 days of the 18-mer peptide into the lateral ventricle of gerbils, starting either 2 h before or immediately after 3 min of forebrain ischemia, protected ischemia-induced learning disability and hippocampal CA1 neuronal loss. Thus, we ascribe the in vitro and in vivo trophic actions of prosaposin on hippocampal neurons to the linear 18-mer sequence and raise the possibility that this peptide can be used as an agent for the treatment of forebrain ischemic damage.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1996.66052197.x
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  • 4
    Electronic Resource
    Electronic Resource
    Two-stage model of incorporation of seamount and oceanic blocks into sedimentary melange: Geochemical and biostratigraphic constraints in Jurassic Chichibu accretionary complex, Shikoku, Japan (1993)
    Oxford, UK : Blackwell Publishing Ltd
    The @island arc 2 (1993), S. 0 
    Details
    ISSN: 1440-1738
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Geosciences
    Notes: Abstract The significance of timing and formation of mélange in accretionary prisms, particularly concerning basaltic and related rocks and pelagic sediments, is exemplified in the Sawadani area of the Jurassic Chichibu accretionary complex in Shikoku, southwest Japan. Major and trace element geochemistry of the basaltic and related rocks indicates that all are of a hot-spot origin which produced a seamount. Most of the rocks have a trend of differentiation from an alkalic parental magma. The time relationship between the blocks and matrices of the mélange deduced from radiolarian fossil evidence and macro- to microscopic characteristics of contacts between different lithologies indicates two stages of mixing of materials in the seafloor. The first mixing occurred on the flank of the seamount in the pelagic environments in the Late Permian, and the second occurred on the trench floor or in the accretionary prism after the Early Jurassic. These two stages show respectively the geological phenomena of a seamount within the Izanagi-Kula plate and its incorporation into the Asian continental margin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1738.1993.tb00071.x
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  • 5
    Electronic Resource
    Electronic Resource
    The gene encoding a newly discovered protein, chorein, is mutated in chorea-acanthocytosis (2001)
    [s.l.] : Nature Publishing Group
    Nature genetics 28 (2001), S. 121-122 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Chorea-acanthocytosis is a neurodegenerative disorder with peripheral red cell acanthocytosis. Linkage of chorea-acanthocytosis to chromosome 9q21 has been found. We refined the locus region and identified a previously unknown, full-length cDNA encoding a presumably structural protein, which we ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/88825
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  • 6
    Electronic Resource
    Electronic Resource
    An immunohistochemical study of basic fibroblast growth factor in the developing chick (1993)
    Springer
    Anatomy and embryology 187 (1993), S. 415-423 
    Details
    ISSN: 1432-0568
    Keywords: Basic fibroblast growth factor ; Immunohistochemistry ; Development ; Chick embryo
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract An antiserum against basic fibrobrast growth factor (bFGF) was characterized by immunoblot experiments and used to investigate immunohistochemically the appearance of bFGF-like immunoreactivity in the developing chick. Crude homogenates of chick embryos at every developmental stage, when subjected to immunoblotting with the use of bFGF antiserum, exhibited a main band with the same molecular weight (18 kDa) as bovine bFGF. With immunohistochemistry, bFGF immunoreactivity (bFGF-IR) was detected exclusively in intracellular components of various tissues at different stages of development; bFGF-IR appeared initially on embryonic (incubation) day 3 (E3) in the myotome, on E12 in the spinal cord and ganglia, on E8 in chondrocytes and osteoblasts of the vertebrae, and on E10 in the esophageal epithelium. Immunoreaction products were present either in the cytoplasm or in the nuclei, depending on the types of individual bFGF-containing cells; developing chondrocytes and cells in the stratum basale of the esophagus exhibited intense immunoreactions exclusively within the nuclei, and the other cells mainly within the cytoplasm. Moreover, bFGF-IR was observed in discrete regions of these tissues at different stages; the epithelium of the esophagus containd bFGF-IR in all layers on E10 to E18 with a superficial-to-basal gradient, but it began to exhibit bFGF-IR only in the stratum basale after E20; and bFGF-IR was more abundant in hypertrophic chondrocytes than in proliferating ones. As chicks aged, bFGF-IR decreased or disappeared in the muscles, vertebrae and esophageal epithelium, but neuronal bFGF increased in intensity until the perinatal period and thereafter remained unchanged. These findings suggest that bFGF not only plays a pivotal role in regulating cell proliferation and differentiation in developing chick tissues, but also acts as a non-mitogenic mediator in nervous tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00174417
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  • 7
    Electronic Resource
    Electronic Resource
    The role of remaining presynaptic terminals in the hippocampal CA1 after selective neuronal death: ischemia-induced glutamate efflux (1995)
    Springer
    Acta neuropathologica 91 (1995), S. 41-46 
    Details
    ISSN: 1432-0533
    Keywords: Key words Glutamate ; Ischemia ; Microdialysis ; Hippocampus ; Cell death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Following selective neuronal death, numerous presynaptic terminals maintain their structural integrity in the brain region. The role that these remaining presynaptic terminals play in the brain region showing selective neuronal death is not known. In the present study, we investigated the possibility that brief transient ischemia induces an excessive release of glutamate from the remaining presynaptic terminals, which then spreads by diffusion. The glutamate could act as an excitotoxin and be a pathogenic factor in the local injured brain region. Transient ischemia of 3.5 min duration was used in the gerbil as a pretreatment to obtain hippocampal CA1 in which most of postsynaptic neurons were eliminated but numerous presynaptic terminals remained normal. At 10–14 days after the pretreatment, brain microdialysis experiments were performed in vivo in the CA1 to measure the levels of extracellular glutamate induced by 5 min ischemia. Prior to 5 min ischemia the basal concentration of glutamate in the CA1 was the same as that observed in gerbils that had been subjected to sham pretreatment. During 5 min ischemia, no significant increase in glutamate was induced in the CA1 which showed selective neuronal death. However, a massive increase in glutamate was induced in the CA1 of the sham-pretreated gerbils. These results suggest that the remaining presynaptic terminals are unlikely to play a pathogenic role in the CA1 after selective neuronal death has occurred.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050390
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  • 8
    Electronic Resource
    Electronic Resource
    Dorsal root ganglion neuron development in chick and rat (1996)
    Springer
    Anatomy and embryology 193 (1996), S. 475-480 
    Details
    ISSN: 1432-0568
    Keywords: Spinal ganglia ; Sensory ganglia ; Pseudo-unipolarization ; Scanning electron microscopy ; Differentiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of this study was to compare the morphological development of dorsal root ganglion neurons in embryonic and early postnatal chicks and rats. The three-dimensional architecture of neurons was observed in ganglia in situ and in dissociated neurons by scanning electron microscopy after removal of the capsule and connective tissue. The percentages of neurons at different developmental stages were determined. The general morphological changes in the chick resembled those in the rat but the timing was different. In both chick and rat, the majority of neurons were bipolar at early stages of development (embryonic day 6 in chick and day 14 in rats) and later underwent pseudo-unipolarization to become mostly unipolar neurons at hatching or birth. This maturation event started at an earlier stage in chick embryos than in rats, with 57% unipolar neurons in chick and only 7% in rat on embryonic day 14. However, just after hatching or birth, at day 22 of development, a larger proportion of immature unipolar neurons remained in chicks (13%) than in rats (3%). We conclude that these differences should be taken into consideration in designing experiments on dorsal root ganglion neurons grown in tissue culture.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00185878
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  • 9
    Electronic Resource
    Electronic Resource
    Changes in guanylate cyclase activity in arteriolar smooth muscle cells and hemodynamics after ischemia-reperfusion in rats (1999)
    Springer
    Acta neuropathologica 98 (1999), S. 603-613 
    Details
    ISSN: 1432-0533
    Keywords: Key words Guanylate cyclase ; Focal cerebral ; ischemia ; Reperfusion ; Hemodynamics ; Microhistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Participation of nitric oxide (NO) and hydroxyl radicals in the pathogenesis of hemodynamic alterations after postischemic recirculation were examined by measuring cerebral blood flow (CBF) and estimating guanylate cyclase activities in arteriolar smooth muscle cells using a reversible 2-h thread occlusion model in rats and an electron microhistochemical technique. In the reversible 2-h ischemia model, guanylate cyclase activity in the arteriolar smooth muscle cells increased at the peak of hyperemia and decreased during postischemic hypoperfusion. Administration of N ω -nitro-l-arginine (L-NNA), a NO synthase inhibitor, in this model decreased infarct volume and completely inhibited both hyperemia and guanylate cyclase activation at hyperemia. Administration of 1,2-bis(nicotinamido)-propane (AVS), a free radical scavenger, affected neither CBF nor guanylate cyclase activity during hyperemia despite a significant reduction in infarct volume. Administration of L-NNA and AVS significantly suppressed the decrease in CBF during postischemic hypoperfusion and the effect of AVS was greater than that of L-NNA. Although continuous infusion of sodium nitroprusside (SNP) following postischemic hypoperfusion in the reversible 2-h ischemia rats without treatment with L-NNA and AVS did not alter either CBF or guanylate cyclase activity, it significantly elevated both CBF and guanylate cyclase activities in rats administered L-NNA and AVS. The responses of CBF and guanylate cyclase to SNP were also greater in AVS- than L-NNA-treated rats. These results suggest that a physiological vasodilative mechanism is involved in the induction of postischemic hyperemia through the NO-guanylate cyclase pathway in arteriolar smooth muscle cells. Both NO-related and non-related radicals are involved in the pathogenesis of postischemic delayed hypoperfusion through the loss of arteriolar smooth muscle relaxation capability.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051125
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  • 10
    Electronic Resource
    Electronic Resource
    Ginseng root prevents learning disability and neuronal loss in gerbils with 5-minute forebrain ischemia (1995)
    Springer
    Acta neuropathologica 91 (1995), S. 15-22 
    Details
    ISSN: 1432-0533
    Keywords: Key words Passive avoidance task ; Delayed neuronal ; death ; Synapse ; Ginseng root ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was designed to investigate the possible neuroprotective activity of ginseng roots in 5-min ischemic gerbils using a step-down passive avoidance task and subsequent neuron and synapse counts in the hippocampal CA1 region. The following drugs were administered for 7 days before the induced ischemia: red ginseng powder (RGP), crude ginseng saponin (CGS), crude ginseng non-saponin (CGNS), and pure ginsenosides Rb1, Rg1 and Ro. Oral administration of RGP significantly prevented the ischemia-induced decrease in response latency, as determined by the passive avoidance test, and rescued a significant number of ischemic hippocampal CA1 pyramidal neurons in a dose-dependent manner. Intraperitoneal injections of CGS exhibited a similar neuroprotective effect. CGNS had a significant but less potent protective effect against impaired passive avoidance task and degeneration of hippocampal CA1 neurons. Ginsenoside Rb1 significantly prolonged the response latency of ischemic gerbils and rescued a significant number of ischemic CA1 pyramidal neurons, whereas ginisenosides Rg1 and Ro were ineffective. Postischemic treatment with RGP, CGS or ginsenoside Rb1 was ineffective. The neuroprotective activities of RGP, CGS and ginsenoside Rb1 were confirmed by electron microscopy counts of synapses in individual strata of the CA1 field of ischemic gerbils pretreated with the drugs. These findings suggest that RGP and CGS are effective in the prevention of delayed neuronal death, and that ginsenoside Rb1 is one of the neuroprotective molecules within ginseng root.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050387
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