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Calcium regulation of the brain-derived neurotrophic factor gene 总被引:13,自引:0,他引:13
Finkbeiner S 《Cellular and molecular life sciences : CMLS》2000,57(3):394-401
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Activation of immediate early genes and memory formation 总被引:14,自引:0,他引:14
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Binglin Zhu Lige Zhao Dong Luo Demei Xu Tao Tan Zhifang Dong Ying Tang Zhuo Min Xiaojuan Deng Fei Sun Zhen Yan Guojun Chen 《Cellular and molecular life sciences : CMLS》2018,75(13):2473-2488
Furin is a proprotein convertase implicated in a variety of pathological processes including neurodegenerative diseases. However, the role of furin in neuronal plasticity and learning and memory remains to be elucidated. Here, we report that in brain-specific furin transgenic (Furin-Tg) mice, the dendritic spine density and proliferation of neural progenitor cells were significantly increased. These mice exhibited enhanced long-term potentiation (LTP) and spatial learning and memory performance, without alterations of miniature excitatory/inhibitory postsynaptic currents. In the cortex and hippocampus of Furin-Tg mice, the ratio of mature brain-derived neurotrophic factor (mBDNF) to pro-BDNF, and the activities of extracellular signal-related kinase (ERK) and cAMP response element-binding protein (CREB) were significantly elevated. We also found that hippocampal knockdown of CREB diminished the facilitation of LTP and cognitive function in Furin-Tg mice. Together, our results demonstrate that furin enhances dendritic morphogenesis and learning and memory in transgenic mice, which may be associated with BDNF–ERK–CREB signaling pathway. 相似文献
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Protein kinases: which one is the memory molecule? 总被引:12,自引:0,他引:12
Encoding of new experiences is likely to induce activity-dependent modifications in the brain. Studies in organisms far apart
on the phylogenetic scale have shown that similar, sometimes identical, signal transduction pathways subserve plasticity in
neuronal systems, and they may play pivotal roles in the formation of long-term memories. It has become evident that phosphorylation/dephosphorylation
reactions are critical for the initiation of cellular mechanisms that embody, retain and modify information in neural circuits.
Although physiological investigations on synaptic plasticity have had a major impact, we have concentrated our review on behavioural
studies that provide direct or indirect evidence for a role of kinases in mechanisms underlying memory formation. From these,
it appears that the learning event induces activation of a variety of kinases with specific time courses. For instance, the
calcium/calmodulin-dependent protein kinase II seems to participate in an early phase of memory formation. Apparently, activation
of both protein tyrosine kinases and mitogen-activated protein kinases is required for much longer and may thus have a particular
function during transformation from short-term into long-term memory. Quite different time courses appear for protein kinase
C (PKC) and protein kinase A (PKA), which may function at two different time points, shortly after training and again much
later. This suggests that PKC and PKA might play a role at early and late stages of memory formation. However, we have considered
some examples showing that these signalling pathways do not function in isolation but rather interact in an intricate intracellular
network. This is indicative of a more complex contribution of each kinase to the fine tuning of encoding and information processing.
To decipher this complexity, pharmacological, biochemical and genetic investigations are more than ever necessary to unravel
the role of each kinase in the syntax of learning and memory formation. 相似文献
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Selenium is an essential trace element. In cattle, selenium deficiency causes dysfunction of various organs, including skeletal
and cardiac muscles. In humans as well, lack of selenium is associated with many disorders, but despite accumulation of clinical
reports, muscle diseases are not generally considered on the list. The goal of this review is to establish the connection
between clinical observations and the most recent advances obtained in selenium biology. Recent results about a possible role
of selenium-containing proteins in muscle formation and repair have been collected. Selenoprotein N is the first selenoprotein
linked to genetic disorders consisting of different forms of congenital muscular dystrophies. Understanding the muscle disorders
associated with selenium deficiency or selenoprotein N dysfunction is an essential step in defining the causes of the disease
and obtaining a better comprehension of the mechanisms involved in muscle formation and maintenance.
Received 13 July 2005; received after revision 9 September 2005; accepted 4 October 2005 相似文献
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The stress-activated protein kinase pathways 总被引:29,自引:0,他引:29
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On a cellular level, formation of memory is based on a selective change in synaptic efficacy that is both fast and, in case
of important information, long-lasting. Rapidity of cellular changes is achieved by modifying preexisting synaptic molecules
(receptors, ion channels), which instantaneously alters the efficacy of synaptic transmission. Endurance, that is the formation
of long-term memory (LTM), is based on transient and perhaps also long-lasting changes in protein synthesis. A number of different
methods exist to interfere with the synthesis of specific proteins or proteins in general. Other methods, in turn, help to
identify proteins whose synthesis is changed following learning. These mostly molecular methods are briefly described in the
present review. Their successful application in a variety of memory paradigms in invertebrates and vertebrates is illustrated.
The data support the importance of selective changes in gene expression for LTM. Proteins newly synthesized during memory
consolidation are likely to contribute to restructuring processes at the synapse, altering the efficiency of transmission
beyond the scope of STM. Increased or, less often, decreased synthesis of proteins appears during specific time windows following
learning. Recent evidence supports older data suggesting that two or even more waves of protein synthesis exist during the
consolidation period. It is expected that the new molecular methods will help to identify and characterize molecules whose
expression changes during LTM formation even in complex vertebrate learning paradigms. 相似文献
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Dysfunction of the mitochondrial respiratory chain has been recognised as a cause of human disease for over 30 years. Advances in the past 10 years have led to a better understanding of the genetics and molecular pathogenesis of many of these disorders. Over 100 primary defects in mitochondrial DNA (mtDNA) are now implicated in the pathogenesis of a group of disorders which are collectively known as the mitochondrial encephalomyopathies, and which most frequently involve skeletal muscle and/or the central nervous system. Although impaired oxidative phosphorylation is likely to be the final common pathway leading to the cellular dysfunction associated with such mtDNA mutations, the complex relationship between genotype and phenotype remains largely unexplained. Most of the genes which encode the respiratory chain reside in the nucleus, yet only five nuclear genes have been implicated in human respiratory chain diseases. There is evidence that respiratory chain dysfunction is present in common neurological diseases such as Parkinson's disease and Huntington's disease. The precise cause of this respiratory chain dysfunction and its relationship to the disease process are unclear. This review focuses upon respiratory chain disorders associated with primary defects in mtDNA. 相似文献
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Zhang X Beaulieu JM Gainetdinov RR Caron MG 《Cellular and molecular life sciences : CMLS》2006,63(1):6-11
Many neuropsychiatric disorders are considered to be related to the dysregulation of brain serotonergic neurotransmission.
Tryptophan hydroxylase-2 (TPH2) is the neuronal-specific enzyme that controls brain serotonin synthesis. There is growing
genetic evidence for the possible involvement of TPH2 in serotonin-related neuropsychiatric disorders; however, the degree of genetic variation in TPH2 and, in particular, its possible functional consequences remain unknown. In this short review, we will summarize some recent
findings with respect to the functional analysis of TPH2.
Received 12 September 2005; received after revision 25 October 2005; accepted 31 October 2005 相似文献
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Protein misfolding and disease: the case of prion disorders 总被引:2,自引:0,他引:2
Recent findings strongly support the hypothesis that diverse human disorders, including the most common neurodegenerative
diseases, arise from misfolding and aggregation of an underlying protein. Despite the good evidence for the involvement of
protein misfolding in disease pathogenesis, the mechanism by which protein conformational changes participate in the disease
is still unclear. Among the best-studied diseases of this group are the transmissible spongiform encephalopathies or prion-related
disorders, in which misfolding of the normal prion protein plays a key role in the disease. In this article we review recent
data on the link between prion protein misfolding and the pathogensis of spongiform encephalopathies.
Received 15 July 2002; received after revision 19 August 2002; accepted 23 August 2002
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ID="*"Corresponding author. 相似文献