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首页> 外文期刊>Neuron >Local presynaptic activity gates homeostatic changes in presynaptic function driven by dendritic BDNF synthesis.
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Local presynaptic activity gates homeostatic changes in presynaptic function driven by dendritic BDNF synthesis.

机译:局部突触前活动门控由树突状BDNF合成驱动的突触前功能的稳态调节。

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摘要

Homeostatic synaptic plasticity is important for maintaining stability of neuronal function, but heterogeneous expression mechanisms suggest that distinct facets of neuronal activity may shape the manner in which compensatory synaptic changes are implemented. Here, we demonstrate that local presynaptic activity gates a retrograde form of homeostatic plasticity induced by blockade of AMPA receptors (AMPARs) in cultured hippocampal neurons. We show that AMPAR blockade produces rapid (<3 hr) protein synthesis-dependent increases in both presynaptic and postsynaptic function and that the induction of presynaptic, but not postsynaptic, changes requires coincident local activity in presynaptic terminals. This "state-dependent" modulation of presynaptic function requires postsynaptic release of brain-derived neurotrophic factor (BDNF) as a retrograde messenger, which is locally synthesized in dendrites in response to AMPAR blockade. Taken together, our results reveal a local crosstalk between active presynaptic terminals and postsynaptic signaling that dictates the manner by which homeostatic plasticity is implemented at synapses.
机译:稳态突触可塑性对于维持神经元功能的稳定性很重要,但是异质表达机制表明神经元活动的不同方面可能会影响代偿性突触变化的实施方式。在这里,我们证明了局部突触前活动门由培养的海马神经元的AMPA受体(AMPARs)的封锁诱导的稳态可塑性的逆行形式。我们表明,AMPAR封锁产生突触前和突触后功能的快速(<3小时)蛋白质合成依赖增加,并且突触前,但不是突触后,变化的诱导需要突触前终端重合的局部活动。突触前功能的这种“状态依赖性”调节,需要突触后释放脑源性神经营养因子(BDNF)作为逆向信使,响应于AMPAR阻断,其在树突中局部合成。两者合计,我们的结果揭示了活跃的突触前终端和突触后信号之间的局部串扰,指示了在突触中实现稳态可塑性的方式。

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