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. Author manuscript; available in PMC: 2012 Nov 19.
Published in final edited form as: Neuron. 2010 Jun 24;66(6):814–816. doi: 10.1016/j.neuron.2010.06.014

Figure 2. Silenced Synapses Are Primed for Potentiation.

Figure 2

Two-photon uncaging of glutamate at single synapses allowed synaptic properties and plasticity to be assessed. Glutamate uncaging at individual spines revealed similar AMPA-receptor-mediated synaptic currents at active and silenced synapses (left panel), but enhanced NMDA receptor synaptic currents at silenced synapses. Weak bursts of glutamate uncaging paired with postsynaptic depolarization (a “subthreshold” stimulus at active synapses, middle panel) produced long-term potentiation and spine enlargement at silenced, but not active, synapses (right panel), likely due to enhanced NMDA EPSCs and greater fractional NR2B at silenced synapses.

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