Synaptic tagging and long-term potentiation - PubMed (original) (raw)
. 1997 Feb 6;385(6616):533-6.
doi: 10.1038/385533a0.
Affiliations
- PMID: 9020359
- DOI: 10.1038/385533a0
Synaptic tagging and long-term potentiation
U Frey et al. Nature. 1997.
Abstract
Repeated stimulation of hippocampal neurons can induce an immediate and prolonged increase in synaptic strength that is called long-term potentiation (LTP)-the primary cellular model of memory in the mammalian brain. An early phase of LTP (lasting less than three hours) can be dissociated from late-phase LTP by using inhibitors of transcription and translation, Because protein synthesis occurs mainly in the cell body, whereas LTP is input-specific, the question arises of how the synapse specificity of late LTP is achieved without elaborate intracellular protein trafficking. We propose that LTP initiates the creation of a short-lasting protein-synthesis-independent 'synaptic tag' at the potentiated synapse which sequesters the relevant protein(s) to establish late LTP. In support of this idea, we now show that weak tetanic stimulation, which ordinarily leads only to early LTP, or repeated tetanization in the presence of protein-synthesis inhibitors, each results in protein-synthesis-dependent late LTP, provided repeated tetanization has already been applied at another input to the same population of neurons. The synaptic tag decays in less than three hours. These findings indicate that the persistence of LTP depends not only on local events during its induction, but also on the prior activity of the neuron.
Comment in
- How do memories leave their mark?
Bear MF. Bear MF. Nature. 1997 Feb 6;385(6616):481-2. doi: 10.1038/385481a0. Nature. 1997. PMID: 9020352 No abstract available.
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