Did the rise in the proportion of labeled axo-spinous synaptic junctions result from local translocation, e.g., the relocation from the nonsynaptic pool of GluR1-containing AMPARs within spines? Alternatively, did the rise in the proportion of labeled synapses involve the influx of GluR1-containing AMPARs from the parent dendritic shafts into spine heads? If the rise resulted from the local, intraspinous translocation only, without the concomitant influx from the parent shaft into spine heads, we would expect to have detected depletion of GluR1 immunoreactivity at nonsynaptic sites within spines. Because we observed no decrease in the proportion of spines labeled at nonsynaptic sites (Fig. 6B), the rise of GluR1 immunoreactivity at synaptic junctions following fear conditioning is likely to have been supported by the influx of GluR1-containing AMPARs from remote shaft sites into nonsynaptic positions within spine heads, to replenish the non-synaptic GluR1-containing AMPAR pool within spine heads that repositioned to the postsynaptic membrane.
