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Published online
doi:10.1083/jcb.200809046
The Journal of Cell Biology, Vol. 185, No. 2, 323-339
The Rockefeller University Press, 0021-9525 $30.00
© Hotulainen et al.
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Article

Defining mechanisms of actin polymerization and depolymerization during dendritic spine morphogenesis



Pirta Hotulainen1,2, Olaya Llano1, Sergei Smirnov1, Kimmo Tanhuanpää1, Jan Faix3, Claudio Rivera1, and Pekka Lappalainen1,2

1 Institute of Biotechnology and 2 Neuroscience Center, University of Helsinki, Helsinki FI-00014, Finland
3 Institute for Biophysical Chemistry, Hannover Medical School, Hannover D-30623, Germany

Correspondence to Pirta Hotulainen: pirta.hotulainen{at}helsinki.fi

Dendritic spines are small protrusions along dendrites where the postsynaptic components of most excitatory synapses reside in the mature brain. Morphological changes in these actin-rich structures are associated with learning and memory formation. Despite the pivotal role of the actin cytoskeleton in spine morphogenesis, little is known about the mechanisms regulating actin filament polymerization and depolymerization in dendritic spines. We show that the filopodia-like precursors of dendritic spines elongate through actin polymerization at both the filopodia tip and root. The small GTPase Rif and its effector mDia2 formin play a central role in regulating actin dynamics during filopodia elongation. Actin filament nucleation through the Arp2/3 complex subsequently promotes spine head expansion, and ADF/cofilin-induced actin filament disassembly is required to maintain proper spine length and morphology. Finally, we show that perturbation of these key steps in actin dynamics results in altered synaptic transmission.

Abbreviations used in this paper: ADF, actin-depolymerizing factor; DIV, days in vitro; mEPSC, miniature excitatory postsynaptic current; V-GLUT-1, vesicular glutamate transporter 1.

© 2009 Hotulainen et al.
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