التفاصيل البيبلوغرافية
| العنوان: |
AP-1/σ1B-adaptin mediates endosomal synaptic vesicle recycling, learning and memory. |
| المؤلفون: |
Glyvuk, Nataliya, Tsytsyura, Yaroslav, Geumann, Constanze, D'Hooge, Rudi, Hüve, Jana, Kratzke, Manuel, Baltes, Jennifer, Böning, Daniel, Klingauf, Jürgen, Schu, Peter |
| المصدر: |
EMBO Journal; 4/7/2010, Vol. 29 Issue 8, p1318-1330, 13p, 1 Diagram, 7 Graphs |
| مصطلحات موضوعية: |
INTELLECTUAL disabilities, DEVELOPMENTAL disabilities, ENDOCYTOSIS, LABORATORY mice, NEURAL circuitry |
| مستخلص: |
Synaptic vesicle recycling involves AP-2/clathrin-mediated endocytosis, but it is not known whether the endosomal pathway is also required. Mice deficient in the tissue-specific AP-1–σ1B complex have impaired synaptic vesicle recycling in hippocampal synapses. The ubiquitously expressed AP-1–σ1A complex mediates protein sorting between the trans-Golgi network and early endosomes. Vertebrates express three σ1 subunit isoforms: A, B and C. The expressions of σ1A and σ1B are highest in the brain. Synaptic vesicle reformation in cultured neurons from σ1B-deficient mice is reduced upon stimulation, and large endosomal intermediates accumulate. The σ1B-deficient mice have reduced motor coordination and severely impaired long-term spatial memory. These data reveal a molecular mechanism for a severe human X-chromosome-linked mental retardation. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
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