TY - JOUR
T1 - Induction of spine growth and synapse formation by regulation of the spine actin cytoskeleton
AU - Zito, Karen
AU - Knott, Graham
AU - Shepherd, Gordon M G
AU - Shenolikar, Shirish
AU - Svoboda, Karel
N1 - Funding Information:
We thank Barry Burbach, John Wallach, and Catherine Zhang for help with experiments; Tom Pologruto and Volker Scheuss for programming; Carey Oliver and Ryan Terry-Lorenzo for sharing data and reagents prior to publication; and Vincenzo De Paola, Ingrid Ehrlich, Anthony Holtmaat, and Alla Karpova for critical reading of the manuscript. This work was supported by the Helen Hay Whitney Foundation (K.Z. was a Merck Fellow), a Burroughs Wellcome Fund Career Award (K.Z.), the Swiss National Science Foundation (G.K.), HHMI (G.M.G.S. and K.S.), and NIH (K.S.).
PY - 2004/10/14
Y1 - 2004/10/14
N2 - We explored the relationship between regulation of the spine actin cytoskeleton, spine morphogenesis, and synapse formation by manipulating expression of the actin binding protein NrbI and its deletion mutants. In pyramidal neurons of cultured rat hippocampal slices, NrbI is concentrated in dendritic spines by binding to the actin cytoskeleton. Expression of one NrbI deletion mutant, containing the actin binding domain, dramatically increased the density and length of dendritic spines with synapses. This hyperspinogenesis was accompanied by enhanced actin polymerization and spine motility. Synaptic strengths were reduced to compensate for extra synapses, keeping total synaptic input per neuron constant. Our data support a model in which synapse formation is promoted by actin-powered motility.
AB - We explored the relationship between regulation of the spine actin cytoskeleton, spine morphogenesis, and synapse formation by manipulating expression of the actin binding protein NrbI and its deletion mutants. In pyramidal neurons of cultured rat hippocampal slices, NrbI is concentrated in dendritic spines by binding to the actin cytoskeleton. Expression of one NrbI deletion mutant, containing the actin binding domain, dramatically increased the density and length of dendritic spines with synapses. This hyperspinogenesis was accompanied by enhanced actin polymerization and spine motility. Synaptic strengths were reduced to compensate for extra synapses, keeping total synaptic input per neuron constant. Our data support a model in which synapse formation is promoted by actin-powered motility.
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U2 - 10.1016/j.neuron.2004.09.022
DO - 10.1016/j.neuron.2004.09.022
M3 - Article
C2 - 15473970
AN - SCOPUS:5144223008
VL - 44
SP - 321
EP - 334
JO - Neuron
JF - Neuron
SN - 0896-6273
IS - 2
ER -