It may also be that synapse strengthening via the increase of GluR1/2-containing AMPARs at synapses formed with the thalamic-plus-cortical axons are counterbalanced by the Arc3.1-mediated efflux of GluR2/3-containing AMPARs at the LA-to-LA synapses or other pathways that remained inactive during fear conditioning. Pathway-specific strengthening, against a background of unchanging or weakened synapses, may be desirable for maintaining homeostasis of LA’s overall excitability. This study focused on measuring changes during STM formation and did not measure changes occurring during the conversion from STM to LTM. The postsynaptic changes that ensue during LTM formation may involve changes in the levels of GluR2/3-containing AMPARs. In particular, it is possible that synapses that have undergone an increase of GluR1-containing AMPARs become strengthened through the insertion of GluR2/3-containing AMPARs during the LTM formation phase. Future studies that quantify GluR2/3 immunoreactivity within spines that are positively identified to be postsynaptic to thalamic and cortical axons would help with testing these working models.
