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[资源] 【资源】Science与Nature-2009年8月21日出品[最新的]

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.
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http://d.namipan.com/d/32c9e8a747c399dbb2c2ff4d9a3670bdad6d6d06d9727001

[ Last edited by zjys5887 on 2009-8-24 at 15:24 ]

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