Optical induction of plasticity at single synapses reveals input-specific accumulation of alphaCaMKII.
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.
Zhang
Yan-Ping
YP
Friedrich Miescher Institute, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.
Holbro
Niklaus
N
Oertner
Thomas G
TG
D000818:Animals; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism*; D003116:Color; D049229:Dendritic Spines / Q000201:enzymology; D018698:Glutamic Acid / Q000378:metabolism; D008027:Light; D021122:Protein Subunits / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013569:Synapses / Q000201:enzymology*; D014796:Visual Perception
D021122:Protein Subunits; D018698:Glutamic Acid; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2