Postsynaptic Membrane Fusion and Long-Term Potentiation
Abstract
The possibility that membrane fusion events in the postsynaptic cell may be required for the change in synaptic strength resulting from long-term potentiation (LTP) was examined. Introducing substances into the postsynaptic cell that block membrane fusion at a number of different steps reduced LTP. Introducing SNAP, a protein that promotes membrane fusion, into cells enhanced synaptic transmission, and this enhancement was significantly less when generated in synapses that expressed LTP. Thus, postsynaptic fusion events, which could be involved either in retrograde signaling or in regulating postsynaptic receptor function or both, contribute to LTP.
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The early phases of LTP/LTD expression are mediated by redistribution of AMPA-type glutamate receptors, with more receptors added to potentiate synapses and receptors removed to weaken synapses.
“The early phases of expression are mediated by a redistribution of AMPA-type glutamate receptors: More receptors are added to potentiate the synapse or receptors are removed to weaken synapses.”
From NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD). (2012) · cites this paper as Lledo et al. 1998
At both silent synapses and synapses that already contain AMPARs, LTP involves the insertion of more AMPARs into the synapse, whereas LTD involves the removal or endocytosis of synaptic AMPARs.
“This result immediately raised the possibility that at both silent synapses and synapses that already contain AMPARs, LTP involves the insertion of more AMPARs into the synapse, whereas conversely, LTD may involve the removal or endocytosis of synaptic AMPARs (Fig. 3) (Lledo et al. 1998;Lu ¨scher et al. 1999).”
From NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD). (2012) · cites this paper as Lledo et al. 1998
Blocking postsynaptic exocytosis by a variety of means blocks LTP/sLTP.
“Numerous studies have shown that blocking postsynaptic exocytosis by a variety of means blocks LTP/sLTP (195, 249, 250, 332–338).”
From Synaptic memory and CaMKII (2023) · cites this paper as [332]
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- Authors
- Lledo, P.-M., Zhang, X., Südhof, T. C., Malenka, R. C., & Nicoll, R. A.
- Affiliations
- Howard Hughes Medical Institute (US)
- P.-M. Lledo, Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143, USA.
- Corresponding author
- Lledo, Pierre-Marie
- Nicoll, Roger A.
- Venue
- Science
- Published
- 1998-01-16
- Volume
- 279
- Issue
- 5349
- Pages
- 399-403
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2033520740
- Cited by
- 413
- References
- 0
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 7 · 2023: 10 · 2022: 7 · 2021: 16 · 2020: 11 · 2019: 9 · 2018: 12 · 2017: 8 · 2016: 10 · 2015: 6 · 2014: 9 · 2013: 14 · 2012: 14
- FWCI
- 16.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- long-term potentiation, synaptic plasticity, synaptic transmission, retrograde signaling, postsynaptic receptors, membrane fusion inhibitors
- MeSH terms
- Amino Acid Sequence, Animals, Botulinum Toxins, Carrier Proteins, Ethylmaleimide, Exocytosis, Guinea Pigs, Hippocampus, Membrane Fusion, Membrane Proteins, Molecular Sequence Data, Synaptic Transmission, Peptides, Recombinant Proteins, Synaptic Membranes, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation, Pyramidal Cells, Patch-Clamp Techniques, Excitatory Postsynaptic Potentials, Vesicular Transport Proteins, N-Ethylmaleimide-Sensitive Proteins, Soluble N-Ethylmaleimide-Sensitive Factor Attachment Proteins, In Vitro Techniques
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