#### [[Synaptic plasticity role in memory]] --- The hippocampus teaches the cortex. LTP occurs through action potential of neuron which expels magnesium and then calcium rushes in and causes CREB/neurotophin to create new synapses. It is generally accepted that the induction of LTP at a synapse requires activation of postsynaptic NMDA receptors through sufficient glutamate release during depolarization. This results in the relief of the voltage-dependent blockage of NMDA receptor by extracellular Mg2+, which in turn permits the entry of Ca2+ into the postsynaptic dendrite spine. Within the dendritic spine, Ca2+ then binds to calmodulin (CaM) to activate CaMKII, which undergoes autophosphorylation, thus maintaining its activity even after Ca2+ returns to basal level. CaMKII phosphorylates AMPA receptors (AMPARs) already present in the synaptic plasma membrane, thus increasing membrane conductance by opening channels. CaMKII is also postulated to influence subsynaptic localization of AMPA receptors in order to recruit more AMPA receptors to the synaptic plasma membrane. --- Tags: Reference: [[@eichenbaumMemory2008]] Related: [[Superlearning MOC]]