Communication Between the Synapse and the Nucleus in Neuronal Development, Plasticity, and Disease

被引:318
作者
Cohen, Sonia [1 ,2 ,3 ,4 ]
Greenberg, Michael F. [1 ,2 ,3 ]
机构
[1] Harvard Univ, Childrens Hosp Boston, EM Kirby Neurobiol Ctr, Sch Med, Boston, MA 02115 USA
[2] Harvard Univ, Dept Neurosurg, Sch Med, Boston, MA 02115 USA
[3] Harvard Univ, Dept Neurobiol, Sch Med, Boston, MA 02115 USA
[4] Harvard Univ, Program Biol & Biomed Sci, Sch Med, Boston, MA 02115 USA
关键词
activity-dependent transcription; calcium; CREB; MEF2; MeCP2; Bdnf;
D O I
10.1146/annurev.cellbio.24.110707.175235
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Sensory experience is critical for the proper development and plasticity of the brain throughout life. Successful adaptation to the environment is necessary, for the survival of an organism, and this process requires the translation of specific sensory stimuli into changes in the structure and function of relevant neural circuits. Sensory-evoked activity drives synaptic input onto neurons within these behavioral circuits, initiating membrane depolarization and calcium influx into the cytoplasm. Calcium signaling triggers the molecular mechanisms underlying neuronal adaptation, including the activity-dependent transcriptional programs that drive the synthesis of the effector molecules required for long-term changes in neuronal function. Insight into the signaling pathways between the synapse and the nucleus that translate specific stimuli into altered patterns of connectivity within a circuit provides clues as to how coordinated and activity-dependent programs of gene expression in how disruptions in this process may contribute to disorders of cognitive function.
引用
收藏
页码:183 / 209
页数:27
相关论文
共 160 条
[1]   Mouse and rat BDNF gene structure and expression revisited [J].
Aid, Tamara ;
Kazantseva, Anna ;
Piirsoo, Marko ;
Palm, Kaia ;
Timmusk, Tonis .
JOURNAL OF NEUROSCIENCE RESEARCH, 2007, 85 (03) :525-535
[2]   Dendrite development regulated by CREST, a calcium-regulated transcriptional activator [J].
Aizawa, H ;
Hu, SC ;
Bobb, K ;
Balakrishnan, K ;
Ince, G ;
Gurevich, I ;
Cowan, M ;
Ghosh, A .
SCIENCE, 2004, 303 (5655) :197-202
[3]   Anatomical and physiological plasticity of dendritic spines [J].
Alvarez, Veronica A. ;
Sabatini, Bernardo L. .
ANNUAL REVIEW OF NEUROSCIENCE, 2007, 30 :79-97
[4]   NFAT dysregulation by increased dosage of DSCR1 and DYRK1A on chromosome 21 [J].
Arron, Joseph R. ;
Winslow, Monte M. ;
Polleri, Alberto ;
Chang, Ching-Pin ;
Wu, Hai ;
Gao, Xin ;
Neilson, Joel R. ;
Chen, Lei ;
Heit, Jeremy J. ;
Kim, Seung K. ;
Yamasaki, Nobuyuki ;
Miyakawa, Tsuyoshi ;
Francke, Uta ;
Graef, Isabella A. ;
Crabtree, Gerald R. .
NATURE, 2006, 441 (7093) :595-600
[5]   REGULATION OF GENE-EXPRESSION IN HIPPOCAMPAL-NEURONS BY DISTINCT CALCIUM SIGNALING PATHWAYS [J].
BADING, H ;
GINTY, DD ;
GREENBERG, ME .
SCIENCE, 1993, 260 (5105) :181-186
[6]   The CBP co-activator is a histone acetyltransferase [J].
Bannister, AJ ;
Kouzarides, T .
NATURE, 1996, 384 (6610) :641-643
[7]   Gene expression profiling of facilitated L-LTP in VP16-CREB mice reveals that BDNF is critical for the maintenance of LTP and its synaptic capture [J].
Barco, A ;
Patterson, S ;
Alarcon, JM ;
Gromova, P ;
Mata-Roig, M ;
Morozov, A ;
Kandell, ER .
NEURON, 2005, 48 (01) :123-137
[8]   Expression of constitutively active CREB protein facilitates the late phase of long-term potentiation by enhancing synaptic capture [J].
Barco, A ;
Alarcon, JM ;
Kandel, ER .
CELL, 2002, 108 (05) :689-703
[9]   The Timothy syndrome mutation differentially affects voltage- and calcium-dependent inactivation of CaV1.2 L-type calcium channels [J].
Barrett, Curtis F. ;
Tsien, Richard W. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2008, 105 (06) :2157-2162
[10]   Variant BDNF (VAl66Met) impact on brain structure and function [J].
Bath, KG ;
Lee, FS .
COGNITIVE AFFECTIVE & BEHAVIORAL NEUROSCIENCE, 2006, 6 (01) :79-85