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【资源】Science与Nature-2009年8月21日出品[最新的]
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Dopamine Controls Persistence of Long-Term Memory Storage Janine I. Rossato, 1,2 Lia R. M. Bevilaqua, 1,2 Iván Izquierdo, 1,2 Jorge H. Medina, 1,3,4 Martín Cammarota1,2,3 * The paradigmatic feature of long-term memory (LTM) is its persistence. However, little is known about the mechanisms that make some LTMs last longer than others. In rats, a long-lasting fear LTM vanished rapidly when the D1 dopamine receptor antagonist SCH23390 was injected into the dorsal hippocampus 12 hours, but not immediately or 9 hours, after the fearful experience. Conversely, intrahippocampal application of the D1 agonist SK38393 at the same critical post-training time converted a rapidly decaying fear LTM into a persistent one. This effect was mediated by brain-derived neurotrophic factor and regulated by the ventral tegmental area (VTA). Thus, the persistence of LTM depends on activation of VTA/hippocampus dopaminergic connections and can be specifically modulated by manipulating this system at definite post-learning time points. 。。。。。。。。。。。。。。。。。 DOI: 10.1126/science.1172545 , 1017 (2009); 325 Science et al. Janine I. Rossato,Memory StorageDopamine Controls Persistence of Long-Term XIAP discriminates between type I and type II FAS-induced apoptosis Philipp J. Jost 1 , Stephanie Grabow1,2 , Daniel Gray1 , Mark D. McKenzie2,3 , Ueli Nachbur 4 , David C. S. Huang1 , Philippe Bouillet 1 , Helen E. Thomas 3 , Christoph Borner 5 , John Silke4 , Andreas Strasser 1 * & Thomas Kaufmann1 FAS (also called APO-1 and CD95) and its physiological ligand, FASL, regulate apoptosis of unwanted or dangerous cells, func- tioning as a guardian against autoimmunity and cancer develop- ment 1–4 . Distinct cell types differ in the mechanisms by which the ‘death receptor’ FAS triggers their apoptosis1–4 . In type I cells, such as lymphocytes, activation of ‘effector caspases’ by FAS-induced activation of caspase-8 suffices for cell killing, whereas in type II cells, including hepatocytes and pancreatic b-cells, caspase cascade amplification through caspase-8-mediated activation of the pro- apoptotic BCL-2 family member BID (BH3 interacting domain death agonist) 5 is essential 6–8 . Here we show that loss of XIAP (X-chromosome linked inhibitor of apoptosis protein ) 9,10 func- tion by gene targeting or treatment with a second mitochondria- derived activator of caspases (SMAC11 , also called DIABLO12 ; direct IAP-binding protein with low pI) mimetic drug in mice rendered hepatocytes and b-cells independent of BID for FAS- induced apoptosis. These results show that XIAP is the critical discriminator between type I and type II apoptosis signalling and suggest that IAP inhibitors should be used with caution in cancer patients with underlying liver conditions. 。。。。。。。。。。。。。。。。。。。。。 http://d.namipan.com/d/32c9e8a74 ... 0bdad6d6d06d9727001 http://d.namipan.com/d/32c9e8a74 ... 0bdad6d6d06d9727001 http://d.namipan.com/d/32c9e8a74 ... 0bdad6d6d06d9727001 http://d.namipan.com/d/32c9e8a747c399dbb2c2ff4d9a3670bdad6d6d06d9727001 [ Last edited by zjys5887 on 2009-8-24 at 15:24 ] |
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