Sensory experience can augment excitatory synaptic strength. Removal of all but one whisker from both sides of the mouse face (single-whisker experience; SWE) leads to an increase in synaptic strength at layer 4-2/3 synapses as well as elevated whisker-evoked fi ring in vivo. Although this potentiation requires NMDAR-activation in its early stages, NMDAR-activation subsequently shift the sign of synaptic change to favor synaptic depression. Thus, timed administration of NMDARantagonists can facilitate experience-dependent increases in excitatory synaptic strength. Here we show that the transition to NMDAR-dependent LTD is transient during ongoing experience-dependent synaptic plasticity in the barrel cortex. Systemic injection of NMDAR-antagonists within the fi rst 12 h of SWE yields a robust enhancement of synaptic strength at layer 4-2/3 synapses. In contrast, later injection (after 36 h of SWE) does not alter synaptic strength compared to vehicle-injected control animals. Thus, as synaptic changes are consolidated by longer periods of whisker plasticity, the window for NMDARdependent synaptic depression closes and strengthened synapses become resilient to biochemical cascades responsible for weakening. Such a process may insure that spurious increases in synaptic strength are not permanently incorporated into cortical networks.
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