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RISS 인기검색어
- 검색키워드
- 저자 : Soderling, Scott H. (검색결과 2 건)
- 무료
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- 유료
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Synaptic Actin Dysregulation, a Convergent Mechanism of Mental Disorders?
Yan, Zhen,Kim, Eunjoon,Datta, Dibyadeep,Lewis, David A.,Soderling, Scott H. Society for Neuroscience 2016 The Journal of neuroscience Vol.36 No.45
<P>Actin polymerization governs activity-dependent modulation of excitatory synapses, including their morphology and functionality. It is clear from humangenetics that neuropsychiatric and neurodevelopmental disturbances are multigenetic in nature, highlighting the need to better understand the critical neural pathways associated with these disorders and how they are altered by genetic risk alleles. One such signaling pathway that is heavily implicated by candidate genes for psychiatric and neurodevelopmental disorders are regulators of signaling to the actin cytoskeleton, suggesting that its disruption and the ensuring abnormalities of spine structures and postsynaptic complexes is a commonly affected pathway in brain disorders. This review will discuss recent experimental findings that strongly support genetic evidence linking the synaptic cytoskeleton to mental disorders, such as schizophrenia and autism spectrum disorders.</P>
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Inositol 1,4,5-trisphosphate 3-kinase a functions as a scaffold for synaptic Rac signaling.
Kim, Il Hwan,Park, Soon Kwon,Hong, Soon Taek,Jo, Yong Sang,Kim, Eun Joo,Park, Eun Hye,Han, Seung Baek,Shin, Hee-Sup,Sun, Woong,Kim, Hyun Taek,Soderling, Scott H,Kim, Hyun The Society 2009 The Journal of neuroscience Vol.29 No.44
<P>Activity-dependent alterations of synaptic contacts are crucial for synaptic plasticity. The formation of new dendritic spines and synapses is known to require actin cytoskeletal reorganization specifically during neural activation phases. Yet the site-specific and time-dependent mechanisms modulating actin dynamics in mature neurons are not well understood. In this study, we show that actin dynamics in spines is regulated by a Rac anchoring and targeting function of inositol 1,4,5-trisphosphate 3-kinase A (IP(3)K-A), independent of its kinase activity. On neural activation, IP(3)K-A bound directly to activated Rac1 and recruited it to the actin cytoskeleton in the postsynaptic area. This focal targeting of activated Rac1 induced spine formation through actin dynamics downstream of Rac signaling. Consistent with the scaffolding role of IP(3)K-A, IP(3)K-A knock-out mice exhibited defects in accumulation of PAK1 by long-term potentiation-inducing stimulation. This deficiency resulted in a reduction in the reorganization of actin cytoskeletal structures in the synaptic area of dentate gyrus. Moreover, IP(3)K-A knock-out mice showed deficits of synaptic plasticity in perforant path and in hippocampal-dependent memory performances. These data support a novel model in which IP(3)K-A is critical for the spatial and temporal regulation of spine actin remodeling, synaptic plasticity, and learning and memory via an activity-dependent Rac scaffolding mechanism.</P>
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