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Addressing the physiological relevance of previous in vitro findings, new behavioural studies have experimentally translated the hypothesis to learning and the consolidation of newly formed memories. These advances call for a revised theory that incorporates the specific molecular and structural processes involved. Additional observations suggest that there are major differences in the mechanisms of functional and structural plasticity. Recent findings, leading us to revise the original hypothesis, indicate that the induction of a local, synapse-specific 'tagged' state and the expression of long-term potentiation are dissociable. Other neural activity, before or after induction, can also determine whether persistent change occurs. The synaptic tagging and capture hypothesis of protein synthesis-dependent long-term potentiation asserts that the induction of synaptic potentiation creates only the potential for a lasting change in synaptic efficacy, but not the commitment to such a change. For example, slow-onset plasticity is explained through tagging without immediate expression, whereby LTP develops as PRPs are captured by non-potentiated but tagged synapses.īehaviourally, weak encoding protocols achieve long-term memory if PRPs are made available by an unrelated event before or after encoding.
#Making memories with series
Taking this into account, the STC can contribute to the understanding of a series of electrophysiological and behavioural phenomena ranging from synaptic plasticity to reconsolidation. In this way, experiments targeting structural plasticity block tagging while allowing the expression of LTP. Recent findings suggest that the induction of the tagged state can be independent of the expression of long-term potentiation (LTP) itself, and this can be explained by differences in the mechanisms of structural and functional plasticity. The synaptic tagging and capture (STC) hypothesis explains this by dissociating synapse-specific tagging from diffusible plasticity-related products (PRPs) - that is, proteins and mRNAs. The fate of a memory is not determined at the time of encoding, and this can be explained by the susceptibility of synaptic plasticity to modulation around the time of induction.
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