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Published Online June 12, 2008
Science DOI: 10.1126/science.1159675

Reports

Submitted on April 28, 2008
Accepted on May 28, 2008

The Spread of Ras Activity Triggered by Activation of a Single Dendritic Spine

Christopher D. Harvey 1{dagger}, Ryohei Yasuda 2{dagger}*, Haining Zhong 1, Karel Svoboda 1*

1 Janelia Farm Research Campus, HHMI, Ashburn, VA 20147, USA.; Watson School of Biological Sciences, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
2 Watson School of Biological Sciences, Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.; Neurobiology Department, Duke University Medical Center, Durham, NC 27710, USA.

* To whom correspondence should be addressed.
Ryohei Yasuda , E-mail: yasuda{at}neuro.duke.edu
Karel Svoboda , E-mail: svobodak{at}janelia.hhmi.org

{dagger}These authors contributed equally to this work.

In neurons, individual dendritic spines isolate NMDA receptor-mediated Ca2+ accumulations from the dendrite and other spines. However, it is not known to what extent spines compartmentalize signaling events downstream of Ca2+ influx. We combined two-photon fluorescence lifetime imaging (FLIM) with two-photon glutamate uncaging to image the activity of the small GTPase Ras following NMDA receptor activation at individual spines. Induction of long-term potentiation (LTP) triggered robust Ca2+-dependent Ras activation in single spines that decayed in approximately 5 minutes. Ras activity spread over approximately 10 micrometers of dendrite and invaded neighboring spines by diffusion. The spread of Ras-dependent signaling was necessary for the local regulation of the threshold for LTP induction. Thus Ca2+-dependent synaptic signals can spread to couple multiple synapses on short stretches of dendrite.


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Science. ISSN 0036-8075 (print), 1095-9203 (online)