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The de novo protein synthesis theory of memory formation is a hypothesis about the formation of the physical correlates of memory in the brain. It is widely accepted that the physiological correlates for memories are stored at the synapse between various neurons .
Protein synthesis plays an important role in the formation of new memories. Studies have shown that protein synthesis inhibitors administered after learning, weaken memory, suggesting that protein synthesis is required for memory consolidation. Additionally, reports have suggested that the effects of protein synthesis inhibitors also inhibit ...
The temporal differentiation between early and late LTP is also based on this. Early LTP is associated with short-term memory and late LTP with long-term memory. Behavioural studies raised evidence against this differentiation. Studies with protein synthesis inhibitors showed that blocking protein synthesis did not block memory retention. [19]
Specifically, it is unclear whether protein synthesis takes place in the postsynaptic cell body or in its dendrites. [39] Despite having observed ribosomes (the major components of the protein synthesis machinery) in dendrites as early as the 1960s, prevailing wisdom was that the cell body was the predominant site of protein synthesis in ...
Memory allocation is a process that determines which specific synapses and neurons in a neural network will store a given memory. [ 1 ] [ 2 ] [ 3 ] Although multiple neurons can receive a stimulus, only a subset of the neurons will induce the necessary plasticity for memory encoding.
By 2015 it had become clear that long-term memory requires gene transcription activation and de novo protein synthesis. [38] Long-term memory formation depends on both the activation of memory promoting genes and the inhibition of memory suppressor genes, and DNA methylation/DNA demethylation was found to be a major mechanism for achieving this ...
Nevertheless, the commonality that exists in every consolidation phase is a short-lived destabilization of a memory object and a susceptibility for said object to react to amnesic agents—principally protein synthesis inhibitors. [5]
Internalization is dependent on protein synthesis, and p120 catenin proteins (p120ctn) are implicated in the turnover, degradation and ‘clustering’ of cadherins into the adhesive junctions at the synapse. [17] P120 ctn proteins are thought to either inhibit endocytosis of neural cadherins, or act at the cell surface to control cadherin ...