Synaptic modifications in cultured hippocampal neurons: Dependence on spike timing, synaptic strength, and postsynaptic cell type
Synaptic modifications in cultured hippocampal neurons: Dependence on spike timing, synaptic strength, and postsynaptic cell type
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DOI：
10.1523/jneurosci.18-24-10464.1998
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发表时间：
1998-12-15
影响因子：
5.3
通讯作者：
Poo, MM
中科院分区：
文献类型：
--
作者：
Bi, GQ;Poo, MM
在分离的大鼠海马神经元的培养中，突触前和突触后神经元的相关尖峰放电可诱导海马能突触的持续增强和抑制。突触前和突触后发放之间的相对时间决定了突触变化的方向和程度。在突触前激活后20毫秒的时间窗口内重复的突触后尖峰导致长时程增强（LTP），而在突触前激活前20毫秒的窗口内的突触后尖峰导致长时程抑制（LTD）。显著的LTP只发生在初始强度较低的突触上，而LTD的程度与初始强度无明显的依赖性。LTP和LTD都依赖于NMDA受体的激活，并且在突触后神经元本质上是GABA能的情况下不存在。用尼莫地平阻断L-型钙通道可阻断LTD的诱导，并降低LTP的程度。这些结果强调的重要性，精确的尖峰时间，突触强度，和突触后细胞类型的活动诱导的修改中央突触，并建议Hebb的规则可能需要纳入一个定量的考虑尖峰时间，反映了狭窄和不对称的窗口诱导突触修改。
In cultures of dissociated rat hippocampal neurons, persistent potentiation and depression of glutamatergic synapses were induced by correlated spiking of presynaptic and postsynaptic neurons. The relative timing between the presynaptic and postsynaptic spiking determined the direction and the extent of synaptic changes. Repetitive postsynaptic spiking within a time window of 20 msec after presynaptic activation resulted in long-term potentiation (LTP), whereas postsynaptic spiking within a window of 20 msec before the repetitive presynaptic activation led to long-term depression (LTD). Significant LTP occurred only at synapses with relatively low initial strength, whereas the extent of LTD did not show obvious dependence on the initial synaptic strength. Both LTP and LTD depended on the activation of NMDA receptors and were absent in cases in which the postsynaptic neurons were GABAergic in nature. Blockade of L-type calcium channels with nimodipine abolished the induction of LTD and reduced the extent of LTP. These results underscore the importance of precise spike timing, synaptic strength, and postsynaptic cell type in the activity-induced modification of central synapses and suggest that Hebb's rule may need to incorporate a quantitative consideration of spike timing that reflects the narrow and asymmetric window for the induction of synaptic modification.