期刊
MOLECULAR BRAIN
卷 4, 期 -, 页码 -出版社
BIOMED CENTRAL LTD
DOI: 10.1186/1756-6606-4-22
关键词
Schaffer collateral synapses RNA transport; late LTP; spontaneous activity-driven potentiation; spine morphogenesis
资金
- Canadian Institutes of Health Research (CIHR Team in Memory Grant) [CTP-79858]
- CIHR [MOP 15121]
- Fonds de la recherche en sante du Quebec (Groupe de recherche sur le systeme nerveux central) [5249]
- Canada Research Chair Program (Canada Research Chair in Cellular and Molecular Neurophysiology) [950-213424]
- Savoy Foundation
Staufens (Stau) are RNA-binding proteins involved in mRNA transport, localization, decay and translational control. The Staufen 1 (Stau1) isoform was recently identified as necessary for the protein synthesis-dependent late phase long-term potentiation (late-LTP) and for the maintenance of mature dendritic spines and synaptic activity in hippocampal CA1 pyramidal cells, strongly suggesting a role of mRNA regulation by Stau1 in these processes. However, the causal relationship between these impairments in synaptic function (spine shape and basal synaptic activity) and plasticity (late-LTP) remains unclear. Here, we determine that the effects of Stau1 knockdown on spine shape and size are mimicked by blocking NMDA receptors (or elevating extracellular Mg2+) and that Stau1 knockdown in the presence of NMDA receptor blockade (or high Mg2+) has no further effect on spine shape and size. Moreover, the effect of Stau1 knockdown on late-LTP cannot be explained by these effects, since when tested in normal medium, slice cultures that had been treated with high Mg2+ (to impair NMDA receptor function) in combination with a control siRNA still exhibited late-LTP, while siRNA to Stau1 was still effective in blocking late-LTP. Our results indicate that Stau1 involvement in spine morphogenesis is dependent on ongoing NMDA receptor-mediated plasticity, but its effects on late-LTP are independent of these changes. These findings clarify the role of Stau1-dependent mRNA regulation in physiological and morphological changes underlying long-term synaptic plasticity in pyramidal cells.
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