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

Ai-Ling Bi1, Yue Wang, Shuang Zhang

  • 1Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, No. 44 Wenhua Xi Road, Jinan, 250012, Shandong, People's Republic of China.

Brain Structure & Function
|December 17, 2013
PubMed

Insights

Memory extinction involves new learning requiring synaptic plasticity. Myosin II regulates actin rearrangement and synaptic changes in the infralimbic cortex, crucial for memory extinction.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Memory extinction, like memory formation, is a learning process dependent on synaptic plasticity.
  • Actin rearrangement is essential for synaptic plasticity, but its role in memory extinction within the infralimbic cortex (IL) is not well understood.

Purpose of the Study:

  • To investigate the role of actin rearrangement in the infralimbic cortex (IL) during memory extinction.
  • To elucidate the underlying molecular mechanisms, focusing on myosin II, in regulating synaptic plasticity during memory extinction.

Main Methods:

  • Utilized a conditioned taste aversion (CTA) paradigm in rodents.
  • Administered inhibitors of actin rearrangement (cytochalasin D) and myosin II (blebbistatin) into the IL.
  • Assessed synaptic density and actin dynamics.
  • Used jasplakinolide to stabilize actin filaments.

Main Results:

  • Synaptic density and actin rearrangement increased in the IL during CTA extinction.
  • Inhibiting actin rearrangement or myosin II function in the IL impaired memory extinction and synapse formation.
  • Myosin II inhibition effects were reversed by stabilizing actin filaments, indicating a role in actin polymerization.

Conclusions:

  • Myosin II regulates actin-related synaptic structure plasticity during memory extinction.
  • This study provides a molecular mechanism for actin rearrangement-associated synaptic plasticity in memory extinction.

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