CaMKIIα is autophosphorylated at the Thr286 site during the acquisition phase of fear conditioning, yielding persistent activity of this kinase (Rodrigues et al., 2004a). Because inhibition of CaMKIIα prevents the NMDAR-dependent form of LTP at thalamic input synapses in the LA, CaMKIIα activation is undoubtedly downstream from NMDAR activation. Both the NMDARs and GluR1-AMPARs lacking GluR2 subunits, as well as the voltage-gated calcium channels, can support the calcium influx necessary to autophosphorylate CaMKIIα. It is possible that some portion of the GluR1-containing AMPARs lack GluR2 subunits. If so, then those GluR1-containing AMPARs that arrive newly to synapses of the paired animals during the earliest phase of STM may contribute, in part, to the calcium influx needed for CaMKIIα activation and LTP in the LA.
