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Eukaryotic initiation factor 2 α-subunit (eIF2α) plays a critical role in the regulation of protein synthesis. Moreover, it also plays an important role in synaptic plasticity and long-term memory consolidation. Sal003 is a selective inhibitor of eIF2α dephosphorylation.

In vitro: Sal003 specifically prevents dephosphorylation of eIF2α by blocking eIF2α phosphatases. In Sal003-treated cells polysomes dissociated and consistent with this β-actin mRNA shifted to lighter fractions, reflecting the inhibition of general translation [1].

In vivo: Intra-basolateral amygdala (BLA) infusions of Sal003 immediately after memory retrieval disrupted the reconsolidation of morphine- or cocaine-induced CPP, leading to a long-lasting suppression of drug-paired stimulus-induced craving. Moreover, inhibition of eIF2α dephosphorylation in the BLA immediately after light/tone stimulus retrieval decreased subsequent cue-induced heroin-seeking behavior in the self-administration procedure. These results demonstrate that eIF2α dephosphorylation in the BLA mediates the memory reconsolidation of drug-paired stimuli [1].

Clinical trials: Currenlty no clinical data are available.

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