Figure 1.

Key molecular mechanisms involved in NMDAR-mediated early LTP. (1) Under basal conditions, calcium (Ca²⁺) ion influx through NMDA receptors (NMDARs) is blocked by magnesium (Mg²⁺) ions in the pore. (2) An increase in neural activity following a specific stimulus pattern leads to enhanced glutamate release from the presynaptic terminal. Subsequently, glutamate binds to NMDARs on the post-synaptic side resulting in an influx of Ca²⁺ resulting in the activation of downstream signaling molecules including CaMKII and PKA promoting the exocytosis and lateral diffusion of AMPARs to the synapse. Spine size and synaptic strength are increased, which are essential for the expression of LTP.