Krucker T, Siggins G R, Halpain S
Departments of Neuropharmacology and Cell Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6856-61. doi: 10.1073/pnas.100139797.
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 microM) 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.
在小鼠海马体的Schaffer侧支-CA1锥体细胞突触处，研究了动态肌动蛋白丝参与突触可塑性特定方面的假说。在细胞外记录场兴奋性突触后电位期间，将低浓度（0.01 - 1 microM）抑制肌动蛋白丝组装的化合物浴用于海马切片。细胞松弛素D、细胞松弛素B和拉特罗毒素A均损害了由短暂高频刺激诱导的长时程增强（LTP）的维持。这种对LTP维持的影响是特异性的，因为这些化合物均不影响基础突触传递、双脉冲易化、LTP诱导或强直后增强。细胞松弛素B的作用是可逆的。这些结果与一个模型一致，即动态肌动蛋白丝在LTP早期维持阶段的分子机制中起重要作用，如新突触连接的生长或沉默突触的转化。
