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树突棘作为协同性长期增强作用的一种机制。

Dendritic spikes as a mechanism for cooperative long-term potentiation.

作者信息

Golding Nace L, Staff Nathan P, Spruston Nelson

机构信息

Department of Neurobiology and Physiology, Institute for Neuroscience, Northwestern University, Evanston, IL 60208-3520, USA.

出版信息

Nature. 2002 Jul 18;418(6895):326-31. doi: 10.1038/nature00854.


DOI:10.1038/nature00854
PMID:12124625
Abstract

Strengthening of synaptic connections following coincident pre- and postsynaptic activity was proposed by Hebb as a cellular mechanism for learning. Contemporary models assume that multiple synapses must act cooperatively to induce the postsynaptic activity required for hebbian synaptic plasticity. One mechanism for the implementation of this cooperation is action potential firing, which begins in the axon, but which can influence synaptic potentiation following active backpropagation into dendrites. Backpropagation is limited, however, and action potentials often fail to invade the most distal dendrites. Here we show that long-term potentiation of synapses on the distal dendrites of hippocampal CA1 pyramidal neurons does require cooperative synaptic inputs, but does not require axonal action potential firing and backpropagation. Rather, locally generated and spatially restricted regenerative potentials (dendritic spikes) contribute to the postsynaptic depolarization and calcium entry necessary to trigger potentiation of distal synapses. We find that this mechanism can also function at proximal synapses, suggesting that dendritic spikes participate generally in a form of synaptic potentiation that does not require postsynaptic action potential firing in the axon.

摘要

赫布提出,突触前和突触后活动同时发生后突触连接的增强是一种学习的细胞机制。当代模型认为,多个突触必须协同作用,以诱导赫布式突触可塑性所需的突触后活动。实现这种协同作用的一种机制是动作电位发放,它始于轴突,但在主动反向传播到树突后可影响突触增强。然而,反向传播是有限的,动作电位常常无法侵入最远端的树突。我们在此表明,海马体CA1锥体神经元远端树突上突触的长期增强确实需要协同的突触输入,但不需要轴突动作电位发放和反向传播。相反,局部产生且空间受限的再生电位(树突棘电位)有助于突触后去极化和钙内流,这是触发远端突触增强所必需的。我们发现这种机制在近端突触也能起作用,这表明树突棘电位通常参与一种不需要轴突中突触后动作电位发放的突触增强形式。

相似文献

[1]
Dendritic spikes as a mechanism for cooperative long-term potentiation.

Nature. 2002-7-18

[2]
A cooperative switch determines the sign of synaptic plasticity in distal dendrites of neocortical pyramidal neurons.

Neuron. 2006-7-20

[3]
Back-propagating action potentials in pyramidal neurons: a putative signaling mechanism for the induction of Hebbian synaptic plasticity.

Restor Neurol Neurosci. 2001

[4]
Synaptic democracy in active dendrites.

J Neurophysiol. 2006-11

[5]
Synaptic integration in tuft dendrites of layer 5 pyramidal neurons: a new unifying principle.

Science. 2009-8-7

[6]
Pathway interactions and synaptic plasticity in the dendritic tuft regions of CA1 pyramidal neurons.

Neuron. 2009-4-16

[7]
Spike-timing-dependent synaptic plasticity depends on dendritic location.

Nature. 2005-3-10

[8]
Dendritic calcium spikes induce bi-directional synaptic plasticity in the lateral amygdala.

Neuropharmacology. 2007-1

[9]
SK (KCa2) channels do not control somatic excitability in CA1 pyramidal neurons but can be activated by dendritic excitatory synapses and regulate their impact.

J Neurophysiol. 2008-11

[10]
Modulation of intracortical synaptic potentials by presynaptic somatic membrane potential.

Nature. 2006-6-8

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[7]
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[9]
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