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Optical induction of plasticity at single synapses reveals input-specific accumulation of alphaCaMKII.


ABSTRACT: Long-term potentiation (LTP), a form of synaptic plasticity, is a primary experimental model for understanding learning and memory formation. Here, we use light-activated channelrhodopsin-2 (ChR2) as a tool to study the molecular events that occur in dendritic spines of CA1 pyramidal cells during LTP induction. Two-photon uncaging of MNI-glutamate allowed us to selectively activate excitatory synapses on optically identified spines while ChR2 provided independent control of postsynaptic depolarization by blue light. Pairing of these optical stimuli induced lasting increase of spine volume and triggered translocation of alphaCaMKII to the stimulated spines. No changes in alphaCaMKII concentration or cytoplasmic volume were observed in neighboring spines on the same dendrite, providing evidence that alphaCaMKII accumulation at postsynaptic sites is a synapse-specific memory trace of coincident activity.

SUBMITTER: Zhang YP 

PROVIDER: S-EPMC2575337 | biostudies-literature | 2008 Aug

REPOSITORIES: biostudies-literature

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Optical induction of plasticity at single synapses reveals input-specific accumulation of alphaCaMKII.

Zhang Yan-Ping YP   Holbro Niklaus N   Oertner Thomas G TG  

Proceedings of the National Academy of Sciences of the United States of America 20080812 33


Long-term potentiation (LTP), a form of synaptic plasticity, is a primary experimental model for understanding learning and memory formation. Here, we use light-activated channelrhodopsin-2 (ChR2) as a tool to study the molecular events that occur in dendritic spines of CA1 pyramidal cells during LTP induction. Two-photon uncaging of MNI-glutamate allowed us to selectively activate excitatory synapses on optically identified spines while ChR2 provided independent control of postsynaptic depolari  ...[more]

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