In contrast, the elevation of profilin was detected within the early time window, like this study—within the first hour following the first pairing of CS and US (Lamprecht et al., 2006a). Therefore, it is plausible to consider that the GluR1-containing AMPARs and profilin interact with one another during the early phase of fear memory formation, as they are both translocated into dendritic spines immediately following fear conditioning. Profilin promotes F-actin elongation and stabilization of spine morphology (Witke, 2004), and is translocated into spine heads of cultured hippocampal neurons in an activity-dependent manner (Ackermann and Matus, 2003; Neuhoff et al., 2005). One possibility is that the enhancement of synaptic strength through the increase of GluR1-containing AMPARs in the LA facilitates profilin influx into spines and this influx of profilin, in turn, stabilizes the F-actin matrix that ramifies the spine head. Stabilized F-actin matrix within spine heads may be one step during STM maintenance and conversion of STM to LTM that facilitates the subsequent trafficking of GluR2/3-containing AMPARs into and out of the spines that have been tagged by the elevated levels of GluR1-containing AMPARs.
