Synaptic plasticity by antidromic firing during hippocampal network oscillations
Synaptic plasticity by antidromic firing during hippocampal network oscillations
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DOI：
10.1073/pnas.1210735110
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发表时间：
2013-03-26
影响因子：
11.1
通讯作者：
Fields, R. Douglas
中科院分区：
文献类型：
--
作者：
Bukalo, Olena;Campanac, Emilie;Fields, R. Douglas
学习和其他认知任务需要将新的经验融入到环境中。相对于感觉诱发的突触可塑性，突触可塑性如何被大脑中的内在活动调节的知之甚少，其中大部分可能涉及神经元放电和整合的非经典模式。海马CA 1区神经元电活动的相干高频振荡[尖波涟漪复合物（SPW-Rs）]在功能上将神经元耦合成瞬时集合。这些振荡发生在慢波睡眠或休息时。参与SPW-R的神经元与相邻的非参与神经元的区别在于，它们在轴突的远端区域异位启动并逆向传播到细胞体的动作电位。GABA（A）介导的轴突去极化和电紧张耦合促进了这种活性。逆向放电对突触强度的可能影响尚不清楚。我们发现，促进自发SPW-Rs在海马切片增加缝隙连接耦合或GABAA介导的轴突去极化导致突触强度的降低，和电刺激轴突引起广泛的，持久的突触抑制。与其他形式的突触可塑性不同，这种突触抑制不依赖于突触输入或谷氨酸受体激活，而是需要L型钙通道激活和功能性间隙连接。逆向放电后传递的突触刺激，否则太弱而不能诱导突触增强，触发了突触强度的持久增加。在SPW-R过程中逆向放电的神经元子集中重新调整突触权重可能有助于通过锐化后续突触输入的特异性和促进新信息的整合来巩固记忆。
Learning and other cognitive tasks require integrating new experiences into context. In contrast to sensory-evoked synaptic plasticity, comparatively little is known of how synaptic plasticity may be regulated by intrinsic activity in the brain, much of which can involve nonclassical modes of neuronal firing and integration. Coherent high-frequency oscillations of electrical activity in CA1 hippocampal neurons [sharp-wave ripple complexes (SPW-Rs)] functionally couple neurons into transient ensembles. These oscillations occur during slow-wave sleep or at rest. Neurons that participate in SPW-Rs are distinguished from adjacent nonparticipating neurons by firing action potentials that are initiated ectopically in the distal region of axons and propagate antidromically to the cell body. This activity is facilitated by GABA(A)-mediated depolarization of axons and electrotonic coupling. The possible effects of antidromic firing on synaptic strength are unknown. We find that facilitation of spontaneous SPW-Rs in hippocampal slices by increasing gap-junction coupling or by GABAA-mediated axon depolarization resulted in a reduction of synaptic strength, and electrical stimulation of axons evoked a widespread, long-lasting synaptic depression. Unlike other forms of synaptic plasticity, this synaptic depression is not dependent upon synaptic input or glutamate receptor activation, but rather requires L-type calcium channel activation and functional gap junctions. Synaptic stimulation delivered after antidromic firing, which was otherwise too weak to induce synaptic potentiation, triggered a long-lasting increase in synaptic strength. Rescaling synaptic weights in subsets of neurons firing antidromically during SPW-Rs might contribute to memory consolidation by sharpening specificity of subsequent synaptic input and promoting incorporation of novel information.