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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1997-01-17
    Beschreibung: Permanent removal of axonal input to postsynaptic cells helps shape the pattern of neuronal connections in response to experience, but the process is poorly understood. Intracellular recording from newborn and adult mouse muscle fibers temporarily innervated by two axons showed an increasing disparity in the synaptic strengths of the two inputs before one was eliminated. The connection that survived gained strength by increasing the amount of neurotransmitter released (quantal content), whereas the input that was subsequently removed became progressively weaker, because of a reduction in quantal content and a reduction in quantal efficacy associated with reduced postsynaptic receptor density. Once the synaptic strengths of two inputs began to diverge, complete axonal withdrawal of the weaker input occurred within 1 to 2 days. These experiments provide a link between experience-driven changes in synaptic strength and long-term changes in connectivity in the mammalian nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Colman, H -- Nabekura, J -- Lichtman, J W -- NS 20364/NS/NINDS NIH HHS/ -- NS 34448/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):356-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Box 8108, Washington University School of Medicine, 660 South Euclid, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8994026" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acetylcholine/metabolism ; Action Potentials ; Aging ; Animals ; Animals, Newborn ; Axons/*physiology ; Electric Stimulation ; Evoked Potentials, Motor ; Mice ; Muscle Fibers, Skeletal/physiology ; Muscle, Skeletal/*innervation ; Neuromuscular Junction/*physiology ; Receptors, Cholinergic/metabolism ; *Synaptic Transmission
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 1996-06-21
    Beschreibung: Insulin-dependent diabetes mellitus (IDDM) is a multigenic autoimmune disease. An IDDM susceptibility gene was mapped to chromosome 2q34. This gene may act early in diabetogenesis, because "preclinical" individuals also showed linkage. Human leukocyte antigen (HLA)-disparate, but not HLA-identical, sibs showed linkage, which was even stronger in families with affected females. The genes encoding insulin-like growth factor-binding proteins 2 and 5 were mapped to a 4-megabase pair interval near this locus. These results indicate the existence of a gene that acts at an early stage in IDDM development, screening for which may identify a specific subset of at-risk individuals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Morahan, G -- Huang, D -- Tait, B D -- Colman, P G -- Harrison, L C -- New York, N.Y. -- Science. 1996 Jun 21;272(5269):1811-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia. morahan@wehi.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8650584" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Alleles ; Animals ; Autoantibodies/analysis ; Chromosome Mapping ; Chromosomes, Human, Pair 2/*genetics ; Diabetes Mellitus, Type 1/*genetics ; Female ; Gene Frequency ; *Genetic Linkage ; *Genetic Markers ; Genetic Predisposition to Disease ; HLA Antigens/genetics ; Humans ; Insulin-Like Growth Factor Binding Protein 2/genetics ; Insulin-Like Growth Factor Binding Protein 5/genetics ; Islets of Langerhans/immunology ; Male ; Mice ; Mice, Inbred NOD/genetics ; Microsatellite Repeats
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
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