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Dynamic actin filaments are required for stable long-term potentiation (LTP) in area CA1 of the hippocampus

机译:动态肌动蛋白丝是海马CA1区稳定长期增强(LTP)所必需的

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摘要

The hypothesis that dynamic actin filaments participate in specific aspects of synaptic plasticity was investigated at the Schaffer-collateral-CA1 pyramidal cell synapse of mouse hippocampus. Low concentrations (0.01–1 μM) of compounds that inhibit actin filament assembly were bath applied to hippocampal slices during extracellular recording of field excitatory postsynaptic potentials. Cytochalasin D, cytochalasin B, and latrunculin A all impaired the maintenance of LTP induced by brief high-frequency stimulation. This effect on LTP maintenance was specific, because none of the compounds affected basal synaptic transmission, paired-pulse facilitation, LTP induction, or post-tetanic potentiation. The effect of cytochalasin B was reversible. The results are consistent with a model in which dynamic actin filaments play an essential role in the molecular mechanisms underlying the early maintenance phase of LTP, such as growth of new synaptic connections or conversion of silent synapses.
机译:动态肌动蛋白丝参与突触可塑性的特定方面的假说在小鼠海马的Schaffer-侧支-CA1锥体细胞突触中进行了研究。在野外兴奋性突触后电位的细胞外记录期间,将抑制肌动蛋白丝装配的低浓度(0.01–1μM)化合物应用于海马切片。细胞松弛素D,细胞松弛素B和latrunculin A均会削弱短暂高频刺激诱导的LTP维持。这种对LTP维持的影响是特定的,因为没有一种化合物会影响基础突触传递,成对脉冲促进,LTP诱导或强直后增强。细胞松弛素B的作用是可逆的。结果与一个模型一致,在该模型中,动态肌动蛋白丝在LTP早期维持阶段的分子机制中起着至关重要的作用,例如新突触连接的生长或沉默突触的转化。

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