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A fearful event forms a strong memory. If recalled, either willingly or not, that memory can change behaviour. To update or weaken or strengthen a memory, it is thought it first becomes destabilised under certain conditions of reactivation. Fear reactivation engages dopamine in the amygdala, but its contribution to reactivation and destabilisation of fear memory is unclear. Dopamine may be a modulator of fear memory processing through its ability to regulate synaptic mechanisms.

Following a combination of behavioural testing (Pavlovian fear-conditioning), pharmacological intervention and molecular analysis in rodents, we found the reactivation of a fear memory activated the Extracellular Regulated Kinase (ERK) pathway in the amygdala downstream of dopamine receptors and may interact with glutamatergic signalling to control distinct stages of memory processing. The results deepen our understanding of the molecular mechanisms downstream of dopamine signalling for reactivation and destabilisation of memories.

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