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  • Wiley  (3)
  • Natural Sciences  (3)
  • 1
    Online Resource
    Online Resource
    Wiley ; 2002
    In:  Annals of the New York Academy of Sciences Vol. 978, No. 1 ( 2002-12), p. 439-454
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 978, No. 1 ( 2002-12), p. 439-454
    Abstract: A bstract : We constructed a realistic simulation model to elucidate whether the characteristics of the cerebellar synaptic plasticity reported in vitro guide the acquisition and adaptation of the ocular following response (OFR). The model reconstructed the firing frequency of the inputs of granule cell axons (GCA), inhibitory cells (IC), and climbing fibers (CF) to cerebellar Purkinje cells for the OFR, to simulate the reported cerebellar plasticity, including long‐term depression, long‐term potentiation, and rebound potentiation. When the model used the same visual inputs as reported for monkeys, it successfully simulated the real characteristics of simple spikes in Purkinje cells of adult monkeys and adaptation of gain and direction. The success of our simulation relied on the temporal relationship of the synaptic weight changes when CF inputs preceded GCA and IC inputs, corresponding to the relationship reported by Chen and Thompson and reanalysis of the data of Karachot et al. The success of our simulation strongly suggests that acquisition and adaptation of the OFR arise from cerebellar plasticity.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2002
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
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  • 2
    Online Resource
    Online Resource
    Wiley ; 2007
    In:  Annals of the New York Academy of Sciences Vol. 1108, No. 1 ( 2007-06), p. 594-602
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1108, No. 1 ( 2007-06), p. 594-602
    Abstract: Abstract :  Immunoinflammatory processes due to chronic infection are thought to be one of the definitive atherogenetic processes. Especially, anti‐heat shock protein antibodies have been related to the prevalence of disease such as coronary artery disease or cerebral infarction, etc., resulted from atherosclerosis. Furthermore, the presence of HSP60‐specific T lymphocytes in circulation may increase the risk of atherosclerosis. We have recently demonstrated the evidences that Helicobacter pylori infection induced atherosclerosis in apoe +/− ldlr +/− mice and that Hp ‐anti‐heat‐shock protein specific Th1‐dominant immune responses had a major involvement in the progression of atherosclerosis. These cellular immune responses caused autoimmunity against endogenous HSP60 (expressed on the stressed cells of vascular endothelium), due to the molecular mimicry. Therefore, an appropriate treatment with antibiotics or with anti‐HSP60 antibodies, which regulates the Th1 induction, could sufficiently reduce the progression of atherosclerosis .
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
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  • 3
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1132, No. 1 ( 2008-06), p. 93-98
    Abstract: Here we present the first evidence that muscle‐specific kinase (MuSK) antigen can cause myasthenia in animals. MuSK is expressed at the postsynaptic membranes of neuromuscular junctions (NMJ) and forms complexes with acetylcholine receptors (AChR) and rapsyn. MuSK is activated by agrin, which is released from motoneurons, and induces AChR clustering and subsequent formation of NMJ in embryos. Notably, autoantibodies against MuSK were found in a proportion of patients with generalized myasthenia gravis (MG) but without the characteristic AChR autoantibodies. However, MuSK autoantibodies had no known pathogenic potential, and animals immunized with purified MuSK proteins did not develop MG in former studies. In contrast, we have now injected rabbits with MuSK ectodomain protein in vivo and evoked a MG‐like muscle weakness with a reduction of AChR clustering at the NMJ. Our results showed that MuSK is required for maintenance of synapses and that interference with that function by MuSK antibodies causes myasthenic weakness. In vitro, AChR clustering in myotubes is induced by agrin and agrin‐independent inducers, which do not activate MuSK. Neither the receptor nor the activation mechanisms of AChR clustering induced by agrin‐independent inducers has been identified with certainty, but MuSK autoantibodies in myasthenic animals inhibited both agrin and agrin‐independent AChR clustering. MuSK plays multiple roles in pre‐patterning of the postsynaptic membrane before innervation and formation of NMJ in embryos. Some of these mechanisms may also participate in the maintenance of mature NMJ. This model system would provide new knowledge about the molecular pathogenesis of MG and MuSK functions in mature NMJ.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2008
    detail.hit.zdb_id: 2834079-6
    detail.hit.zdb_id: 211003-9
    detail.hit.zdb_id: 2071584-5
    SSG: 11
    Location Call Number Limitation Availability
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