NMDARs, minimal Ca2+ influx, and a reduction in post-synaptic AMPA surface receptor density via dynamin- and clathrin-dependent endocytosis (Malenka and Bear, 2004). Much of the NMDAR-dependent plasticity has focused on mechanisms responsible for the initial increase in synaptic strength, however the long-lasting biological effects likely require new protein synthesis and gene transcription (Lynch, 2004). There are quantifiable alterations in the morphology of dendrites and dendritic spines that accompany LTP (Andersen and Soleng, 1998; Yuste and Bonhoeffer, 2001; Matsuzaki et al., 2004) and together these long-lasting changes have been implicated as an essential mechanism and molecular basis for learning and memory. Additionally, there are other modulators of plasticity, such as metabotropic glutamate receptors and endocannabinoids, that have been discovered and reviewed extensively elsewhere [see review, Kauer and Malenka (2007)].
