Synaptic plasticity likely involves a plethora of synaptic molecules (Malenka and Bear, 2004). Of these, previous studies highlighted GluR1 as one synaptic protein whose level at synapses becomes augmented following fear conditioning (Rumpel et al., 2005; Yeh et al., 2006). These previous studies detected increases in synaptic AMPAR currents carried by exogenous recombinant genes by the third hour after fear onditioning (Rumpel et al., 2005) and of endogenous surface AMPAR, as assessed by Western blotting, by the second hour following fear conditioning (Yeh et al., 2006). To date, our study is the first to focus on the formation of short-term memory (STM) of fear by analyzing the distribution of receptor subunits at synapses within 40 minutes following fear conditioning. Our results support and extend previous findings by confirming that endogenous GluR1-containing AMPARs, like the GFP-tagged GluR1-containing AMPARs (Rumpel et al., 2005), increase at LA synapses following fear conditioning. The ultrastructural data reveal that GluR1-containing AMPARs rise earlier than reported previously (Rumpel et al., 2005; Yeh et al., 2006). This difference is likely to be due to the greater sensitivity with which ultrastructural data can detect changes in the number of synapses expressing GluR1-containing AMPARs precisely at the synaptic junction.
