共 2 条
- [1] The Roles of CaMKII and F-Actin in the Structural Plasticity of Dendritic Spines: A Potential Molecular Identity of a Synaptic Tag?PHYSIOLOGY, 2009, 24 (06) : 357 - 366Okamoto, KenichiBosch, MiquelHayashi, Yasunori
A Temporary Gating of Actin Remodeling during Synaptic Plasticity Consists of the Interplay between the Kinase and Structural Functions of CaMKII
被引：106
|作者：
Kim, Karam
[1
]
Lakhanpal, Gurpreet
[2
]
Lu, Hsiangmin E.
[3
,4
]
Khan, Mustafa
[2
]
Suzuki, Akio
[1
]
Kato-Hayashi, Mariko
[6
]
Narayanan, Radhakrishnan
[6
]
Luyben, Thomas T.
[2
,7
]
Matsuda, Tomoki
[8
]
Nagai, Takeharu
[8
]
Blanpied, Thomas A.
[3
,4
,5
]
Hayashi, Yasunori
[1
,6
,9
,10
]
Okamoto, Kenichi
[2
,6
,7
]
机构：
[1] RIKEN, Brain Sci Inst, Wako, Saitama 3510198, Japan
[2] Mt Sinai Hosp, Lunenfeld Tanenbaum Res Inst, Toronto, ON M5G 1X5, Canada
[3] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA
[4] Univ Maryland, Sch Med, Program Mol Med, Baltimore, MD 21201 USA
[5] Univ Maryland, Sch Med, Program Neurosci, Baltimore, MD 21201 USA
[6] MIT, Dept Brain & Cognit Sci, Picower Inst Learning & Memory, RIKEN MIT Neurosci Res Ctr, Cambridge, MA 02139 USA
[7] Univ Toronto, Fac Med, Dept Mol Genet, Toronto, ON M5S 1A8, Canada
[8] Osaka Univ, Inst Sci & Ind Res, Osaka 5670047, Japan
[9] Saitama Univ, Brain & Body Syst Sci Inst, Saitama 3388570, Japan
[10] S China Normal Univ, Sch Life Sci, Guangzhou 510631, Guangdong, Peoples R China
来源：
基金：
加拿大创新基金会;
关键词：
LONG-TERM POTENTIATION;
SINGLE DENDRITIC SPINES;
F-ACTIN;
HIPPOCAMPAL-NEURONS;
AMPA RECEPTORS;
BETA;
SYNAPSES;
DYNAMICS;
PROTEIN;
ACTIVATION;
D O I：
10.1016/j.neuron.2015.07.023
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
The structural modification of dendritic spines plays a critical role in synaptic plasticity. CaMKII is a pivotal molecule involved in this process through both kinase-dependent and independent structural functions, but the respective contributions of these two functions to the synaptic plasticity remain unclear. We demonstrate that the transient interplay between the kinase and structural functions of CaMKII during the induction of synaptic plasticity temporally gates the activity-dependent modification of the actin cytoskeleton. Inactive CaMKII binds F-actin, thereby limiting access of actin-regulating proteins to F-actin and stabilizing spine structure. CaMKII-activating stimuli trigger dissociation of CaMKII from F-actin through specific autophosphorylation reactions within the F-actin binding region and permits F-actin remodeling by regulatory proteins followed by reassociation and restabilization. Blocking the autophosphorylation impairs both functional and structural plasticity without affecting kinase activity. These results underpin the importance of the interplay between the kinase and structural functions of CaMKII in defining a time window permissive for synaptic plasticity.
引用
收藏
页码：813 / 826
页数：14
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