The cellular basis of memory involves _activity dependent plasticity_ in synaptic connections. An important model in the study of the cellular basis of memory is the phenomenon of _long-term potentiation_ (LTP), a long-lasting increase in the strength of a synaptic response following stimulation (Bliss et al., 2007). LTP is prominent in the hippocampus, as well as in the cerebral cortex and other brain areas that are involved in different forms of memory. LTP is typically induced by the co-occurence of excitatory input and intracellular depolarization at the so-called _[Hebbian](http://www.scholarpedia.org/article/Donald_Olding_Hebb "Donald Olding Hebb") synapse_, involving N-methyl-d-aspartate (NMDA) receptors that allow the entry of Ca++ into the synapse, which activates cyclic adenosine monophosphate (cAMP). Subsequently, cAMP activates several kinases, some of which increase the number of synaptic receptors. In addition, cAMP activates cAMP-response element binding protein (CREB), which operates within the nucleus to activate a class of genes called immediate early genes, which, in turn, activate other genes that direct protein synthesis. Among the proteins produced is neurotrophin, which activates growth of the synapse. Thus, a series of molecular reactions plays a vital role in fixating the changes in synaptic function that occur in LTP.