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. Author manuscript; available in PMC: 2013 Aug 1.
Published in final edited form as: Neurosci Biobehav Rev. 2011 Nov 7;36(7):1750–1762. doi: 10.1016/j.neubiorev.2011.11.001

Figure 2. Schematic diagram depicting a theoretical model of how the basolateral complex of the amygdala (BLA) modulates synaptic plasticity in the hippocampus.

Figure 2

Contextual/sensory input initiates transcription of the immediate early gene Arc in pyramidal cells of the CA1 region of the dorsal hippocampus. Arc mRNA is transported to the postsynaptic density of synapses stimulated by the novel context. In position to modify engaged synapses, Arc is either translated to protein, and can thus affect the strength of the synapse, or it is degraded. The coincident and long-lasting amygdala response to stress hormones contributes, directly or indirectly (through entorhinal cortex or septal region), to protein synthesis-dependent changes that underlie long-term plasticity and memory by influencing the translation or degredation of Arc, and possibly other plasticity-related proteins. (Hippocampus illustration, Cajal, 1911).