4.8 Article

Myosin IIb Regulates Actin Dynamics during Synaptic Plasticity and Memory Formation

期刊

NEURON
卷 67, 期 4, 页码 603-617

出版社

CELL PRESS
DOI: 10.1016/j.neuron.2010.07.016

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资金

  1. UAB
  2. McKnight Brain Institute
  3. Alabama Health Sciences Foundation
  4. National Institute of Neurological Disorders (NINDS) [NS064079, N505182, NS45260, 045540]
  5. National Institute of Mental Health [MH083396]
  6. National Institute on Aging [AG00096]
  7. Kauffman Foundation

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Reorganization of the actin cytoskeleton is essential for synaptic plasticity and memory formation. Presently, the mechanisms that trigger actin dynamics during these brain processes are poorly understood. In this study, we show that myosin II motor activity is downstream of LTP induction and is necessary for the emergence of specialized actin structures that stabilize an early phase of LTP. We also demonstrate that myosin II activity contributes importantly to an actin-dependent process that underlies memory consolidation. Pharmacological treatments that promote actin polymerization reversed the effects of a myosin II inhibitor on LTP and memory. We conclude that myosin II motors regulate plasticity by imparting mechanical forces onto the spine actin cytoskeleton in response to synaptic stimulation. These cytoskeletal forces trigger the emergence of actin structures that stabilize synaptic plasticity. Our studies provide a mechanical framework for understanding cytoskeletal dynamics associated with synaptic plasticity and memory formation.

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