Timing in synaptic plasticity: from detection to integration

被引:56
作者
Bi, GQ [1 ]
Rubin, J
机构
[1] Univ Pittsburgh, Sch Med, Dept Neurobiol, Pittsburgh, PA 15261 USA
[2] Univ Pittsburgh, Sch Med, Ctr Nueral Basis Cognit, Pittsburgh, PA 15261 USA
[3] Univ Pittsburgh, Dept Math, Pittsburgh, PA 15260 USA
[4] Univ Pittsburgh, Ctr Neural Basis Cognit, Pittsburgh, PA 15261 USA
关键词
D O I
10.1016/j.tins.2005.02.002
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Timing of cellular and subcellular events contributes to spiking-induced modification of synapses in a variety of ways. Initially, the timing of presynaptic and postsynaptic action potentials must be translated into signals that can initiate intracellular processes. Recent experimental and computational findings suggest that the spatiotemporal details of such signals, in particular the time courses and locations of postsynaptic Ca2+ transients, might themselves be crucial for driving potentiation and depression modules that interact in a time-dependent way to determine plasticity outcomes. On longer timescales, the effects of multiple spikes are integrated in a nonlinear manner, yielding non-intuitive plasticity results that are likely to be sensitive to local conditions and, finally, additional elements must be called into action to stabilize changes in synaptic strengths. This review is part of the TINS Synaptic Connectivity series.
引用
收藏
页码:222 / 228
页数:7
相关论文
共 70 条
[11]   Synaptic modifications in cultured hippocampal neurons: Dependence on spike timing, synaptic strength, and postsynaptic cell type [J].
Bi, GQ ;
Poo, MM .
JOURNAL OF NEUROSCIENCE, 1998, 18 (24) :10464-10472
[12]   A SYNAPTIC MODEL OF MEMORY - LONG-TERM POTENTIATION IN THE HIPPOCAMPUS [J].
BLISS, TVP ;
COLLINGRIDGE, GL .
NATURE, 1993, 361 (6407) :31-39
[13]   Sensitivity of CaM kinase II to the frequency of Ca2+ oscillations [J].
De Koninck, P ;
Schulman, H .
SCIENCE, 1998, 279 (5348) :227-230
[14]   Long-term synaptic plasticity between pairs of individual CA3 pyramidal cells in rat hippocampal slice cultures [J].
Debanne, D ;
Gähwiler, BH ;
Thompson, SM .
JOURNAL OF PHYSIOLOGY-LONDON, 1998, 507 (01) :237-247
[15]   Signaling to the nucleus by an L-type calcium channel - Calmodulin complex through the MAP kinase pathway [J].
Dolmetsch, RE ;
Pajvani, U ;
Fife, K ;
Spotts, JM ;
Greenberg, ME .
SCIENCE, 2001, 294 (5541) :333-339
[16]  
Feldman DE, 1999, J NEUROBIOL, V41, P92, DOI 10.1002/(SICI)1097-4695(199910)41:1<92::AID-NEU12>3.3.CO
[17]  
2-L
[18]   Complexity of calcium signaling in synaptic spines [J].
Franks, KM ;
Sejnowski, TJ .
BIOESSAYS, 2002, 24 (12) :1130-1144
[19]   An MCell model of calcium dynamics and frequency-dependence of calmodulin activation in dendritic spines [J].
Franks, KM ;
Bartol, TM ;
Sejnowski, TJ .
NEUROCOMPUTING, 2001, 38 :9-16
[20]   Spike-timing-dependent synaptic modification induced by natural spike trains [J].
Froemke, RC ;
Dan, Y .
NATURE, 2002, 416 (6879) :433-438