Myosin II regulates actin rearrangement-related structural synaptic plasticity during conditioned taste aversion memory extinction
Myosin II regulates actin rearrangement-related structural synaptic plasticity during conditioned taste aversion memory extinction
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肌球蛋白 II 在条件性味觉厌恶记忆消退过程中调节肌动蛋白重排相关的结构突触可塑性
DOI：
10.1007/s00429-013-0685-5
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发表时间：
2015-03-01
影响因子：
3.1
通讯作者：
Chen, Zhe-Yu
中科院分区：
文献类型：
--
作者：
Bi, Ai-Ling;Wang, Yue;Chen, Zhe-Yu
与记忆形成类似，记忆消退也是一种新的学习过程，需要突触的可塑性。肌动蛋白重排是突触可塑性的基础，然而，肌动蛋白重排在边缘下皮层（IL）是否在记忆消退中起作用，以及其潜在的机制尚不清楚。在这里，使用条件味觉厌恶（CTA）范式，我们证明了在CTA消失期间，IL中的突触密度和肌动蛋白重排增加。靶向输注肌动蛋白重排抑制剂细胞松弛素D，使记忆消退和新生突触形成受损。值得注意的是，我们还发现在CTA消失期间IL中肌球蛋白II磷酸化增加。将肌球蛋白II atp酶的特异性抑制剂blebbistatin （Blebb）微量注入IL受损的记忆消退以及相关的肌动蛋白重排和突触密度的变化。此外，肌动蛋白聚合稳定剂jasplakinolide （Jasp）可以挽救Blebb引起的消光缺陷和突触密度的降低，这表明肌动蛋白II在CTA消光过程中通过肌动蛋白丝聚合来稳定突触可塑性。综上所述，我们得出结论，肌球蛋白II可能调节记忆消退过程中肌动蛋白相关突触结构的可塑性。我们的研究为理解记忆消退过程中肌动蛋白重排相关突触结构的可塑性提供了分子机制。
Similar to memory formation, memory extinction is also a new learning process that requires synaptic plasticity. Actin rearrangement is fundamental for synaptic plasticity, however, whether actin rearrangement in the infralimbic cortex (IL) plays a role in memory extinction, as well as the mechanisms underlying it, remains unclear. Here, using a conditioned taste aversion (CTA) paradigm, we demonstrated increased synaptic density and actin rearrangement in the IL during the extinction of CTA. Targeted infusion of an actin rearrangement inhibitor, cytochalasin D, into the IL impaired memory extinction and de novo synapse formation. Notably, we also found increased myosin II phosphorylation in the IL during the extinction of CTA. Microinfusion of a specific inhibitor of the myosin II ATPase, blebbistatin (Blebb), into the IL impaired memory extinction as well as the related actin rearrangement and changes in synaptic density. Moreover, the extinction deficit and the reduction of synaptic density induced by Blebb could be rescued by the actin polymerization stabilizer jasplakinolide (Jasp), suggesting that myosin II acts via actin filament polymerization to stabilize synaptic plasticity during the extinction of CTA. Taken together, we conclude that myosin II may regulate the plasticity of actin-related synaptic structure during memory extinction. Our studies provide a molecular mechanism for understanding the plasticity of actin rearrangement-associated synaptic structure during memory extinction.