Cofilin Activation Is Temporally Associated with the Cessation of Growth in the Developing Hippocampus.

Authors: Lauterborn, JC  Kramar, EA  Rice, JD  Babayan, AH  Cox, CD  Karsten, CA  Gall, CM  Lynch, G 
Citation: Lauterborn JC, etal., Cereb Cortex. 2016 Apr 12. pii: bhw088.
Pubmed: (View Article at PubMed) PMID:27073215
DOI: Full-text: DOI:10.1093/cercor/bhw088

Dendritic extension and synaptogenesis proceed at high rates in rat hippocampus during early postnatal life but markedly slow during the third week of development. The reasons for the latter, fundamental event are poorly understood. Here, we report that levels of phosphorylated (inactive) cofilin, an actin depolymerizing factor, decrease by 90% from postnatal days (pnds) 10 to 21. During the same period, levels of total and phosphorylated Arp2, which nucleates actin branches, increase. A search for elements that could explain the switch from inactive to active cofilin identified reductions in beta1 integrin, TrkB, and LIM domain kinase 2b, upstream proteins that promote cofilin phosphorylation. Moreover, levels of slingshot 3, which dephosphorylates cofilin, increase during the period in which growth slows. Consistent with the cofilin results, in situ phalloidin labeling of F-actin demonstrated that spines and dendrites contained high levels of dynamic actin filaments during Week 2, but these fell dramatically by pnd 21. The results suggest that the change from inactive to constitutively active cofilin leads to a loss of dynamic actin filaments needed for process extension and thus the termination of spine formation and synaptogenesis. The relevance of these events to the emergence of memory-related synaptic plasticity is described.


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CRRD Object Information
CRRD ID: 11568695
Created: 2016-12-13
Species: All species
Last Modified: 2016-12-13
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.