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Synaptic plasticity is thought to contribute to memory formation.Serotonin-induced facilitation of sensory-motor (SN-MN) synapses in Aplysia  is an extensively studied cellular analog of memory forsensitization. Serotonin, a modulatory neurotransmitter, is released in theCNS during sensitization training, and induces three temporally andmechanistically distinct phases of SN-MN synaptic facilitation. The role ofprotein kinase A and protein kinase C in SN-MN synaptic facilitation is welldocumented. Recently, it has become clear that mitogen-activated proteinkinase (MAPK) cascades also play a critical role in SN-MN plasticity. Here, wesummarize the roles of MAPK cascades in synaptic plasticity and memory forsensitization in  Aplysia .

The Roles of MAPK Cascades in Synaptic Plasticity and Memory in Aplysia: Facilitatory Effects and Inhibitory Constraints: Figure 1