Figure 6.

A model of consolidation of conditioning and consolidation of extinction of memory in the amygdala. Both acquisition and extinction trigger calcium influx through either NMDA receptors or L-type calcium channels in the amygdala. The increase in intracellular Ca²⁺ leads to the activation of protein kinases (e.g., PKA, PI-3 kinase, and MAPK). The activated kinases then translocate into the nucleus in which they phosphorylate CREB to initiate gene transcription and translation. Extinction training not only reactivates original memory this way but also promotes calcineurin synthesis via the existed mRNA. Calcineurin then exerts a negative feedback effect to dephosphorylate kinases and weakens the original memory. Thus, the outcome of the effect of protein synthesis inhibition on the reconsolidation-extinction may depend on a competition between these two processes.