title: Phosphorylation of cofilin regulates extinction of conditioned aversive memory via AMPAR trafficking.
abstract: Actin dynamics provide an important mechanism for the modification of synaptic plasticity, which is regulated by the actin depolymerizing factor (ADF)/cofilin. However, the role of cofilin regulated actin dynamics in memory extinction process is still unclear. Here, we observed that extinction of conditioned taste aversive (CTA) memory led to temporally enhanced ADF/cofilin activity in the infralimbic cortex (IrL) of the rats. Moreover, temporally elevating ADF/cofilin activity in the IrL could accelerate CTA memory extinction by facilitating AMPAR synaptic surface recruitment, whereas inhibition of ADF/cofilin activity abolished AMPAR synaptic surface trafficking and impaired memory extinction. Finally, we observed that ADF/cofilin-regulated synaptic plasticity was not directly coupled to morphological changes of postsynaptic spines. These findings may help us understand the role of ADF/cofilin-regulated actin dynamics in memory extinction and suggest that appropriate manipulating ADF/cofilin activity might be a suitable way for therapeutic treatment of memory disorders.
authors.affiliation: Department of Neurobiology, Shandong Provincial Key Laboratory of Mental Disorders, School of Medicine, Shandong University, Jinan, Shandong 250012, People's Republic of China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Wang
authors.forename: Qing
authors.initials: Q
authors.lastname: Dong
authors.forename: Xu-Feng
authors.initials: XF
authors.lastname: Xu
authors.forename: Xuan
authors.initials: X
authors.lastname: Feng
authors.forename: Jian
authors.initials: J
authors.lastname: Xin
authors.forename: Dong-Dong
authors.initials: DD
authors.lastname: Wang
authors.forename: Hui
authors.initials: H
authors.lastname: Yu
authors.forename: Tian
authors.initials: T
authors.lastname: Tian
authors.forename: Zhe-Yu
authors.initials: ZY
authors.lastname: Chen
mesh_terms: D051339:Actin Depolymerizing Factors / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D003213:Conditioning, Psychological / Q000502:physiology; D049229:Dendritic Spines / Q000648:ultrastructure; D005108:Extinction, Psychological / Q000502:physiology*; D054461:Lim Kinases / Q000378:metabolism / Q000502:physiology*; D008032:Limbic System / Q000378:metabolism / Q000502:physiology; D008297:Male; D008840:Microfilament Proteins / Q000378:metabolism / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism / Q000502:physiology*; D010766:Phosphorylation; D021381:Protein Transport / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D018091:Receptors, AMPA / Q000378:metabolism / Q000502:physiology*
chemical_list: D051339:Actin Depolymerizing Factors; D054461:Lim Kinases; D008840:Microfilament Proteins; D010744:Phosphoric Monoester Hydrolases; D018091:Receptors, AMPA; C515894:Limk1 protein, rat; C529152:SSH1 protein, rat; C104722:glutamate receptor ionotropic, AMPA 2