We review recent work on three major lines of memory research: a) the possible role of the protein kinase M-zeta (PKMzeta) in memory persistence; b) the processes of “synaptic tagging and capture” in memory formation; c) the modulation of extinction learning, widely used in the psychotherapy of fear memories under the name of “exposure therapy”. PKMzeta is a form of protein kinase C (PKC) that apparently remains stimulated for months after the consolidation of a given memory. Synaptic tagging is a mechanism whereby the weak activation of one synapse can tag it with a protein so other synapses in the same cell can reactivate it by producing other proteins that bind to the tag. Extinction, once mistakenly labeled as a form of forgetting, is by itself a form of learning; through it animals can learn to inhibit a response. We now know it can be modulated by neurotransmitters or by synaptic tagging, which should enable better control of its clinical use.

A evocação labiliza os arquivos de memória, e isto permite dois processos dependentes de síntese protéica no cérebro: a extinção, que inibe a evocação ulterior, e a reconsolidação, que pode aumentar a evocação ou mudar seu conteúdo. A extinção pode por sua vez sofrer reconsolidação. Interações entre estes dois processos podem ser aplicados ao tratamento das memórias de medo, tais como aquelas em que se baseia o estresse pós-traumático.

Retrieval labilizes memory traces and these gates two protein synthesis-dependent processes in the brain: extinction, which inhibits further retrieval, and reconsolidation, which may enhance retrieval or change its content. Extinction may itself suffer reconsolidation. Interactions among these processes may be applied to treatments of fear memories, such as those underlying post-traumatic stress disorders.