Double-label confocal microscopy of phosphorylated protein kinases involved in long-term potentiation

There are a number of phenomenological features of memory that must have parallels at the synaptic/cellular level. Among the most important of these attributes is the ability to establish a learned modification relatively quickly and to have it persist over a relatively long period. The best candidate for a cellular mechanism by which synaptic strength is increased as a consequence of experience is long-term potentiation (LTP). Most plastic synapses in the central nervous system employ glutamate as their neurotransmitter and current models of LTP propose that the activation of N-methyl-D-aspartate (NMDA) channels is critical for the influx of Ca2+ into the postsynaptic cell. The increased postsynaptic concentration of Ca 2+ activates a variety of calcium-binding proteins, such as adenylyl cyclase, protein kinase C (PKC), calmodulin kinase II (CaMKII), and others.