Myosin II regulates actin rearrangement-related structural synaptic plasticity during conditioned taste aversion memory extinction

Brain Structure & Function
Ai-Ling BiZhe-Yu Chen

Abstract

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...Continue Reading

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Citations

Jul 12, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Andrés Molero-Chamizo, Guadalupe Nathzidy Rivera-Urbina
Nov 23, 2017·Frontiers in Molecular Neuroscience·Adonis Yiannakas, Kobi Rosenblum
Jun 18, 2021·Investigative Ophthalmology & Visual Science·Ai-Ling BiHong-Sheng Bi

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