A Single Brief Burst Induces GluR1-dependent Associative Short-term Potentiation: A Potential Mechanism for Short-term Memory
Open accessAbstract
Recent work showed that short-term memory (STM) is selectively reduced in GluR1 knockout mice. This raises the possibility that a form of synaptic modification dependent on GluR1 might underlie STM. Studies of synaptic plasticity have shown that stimuli too weak to induce long-term potentiation induce short-term potentiation (STP), a phenomenon that has received little attention. Here we examined several properties of STP and tested the dependence of STP on GluR1. The minimal requirement for inducing STP was examined using a test pathway and a conditioning pathway. Several closely spaced stimuli in the test pathway, forming a single brief burst, were sufficient to induce STP. Thus, STP is likely to be induced by the similar bursts that occur in vivo. STP induction is associative in nature and dependent on the NMDAR. STP decays with two components, a fast component (1.6 ± 0.26 min) and a slower one (19 ± 6.6 min). To test the role of GluR1 in STP, experiments were conducted on GluR1 knockout mice. We found that STP was greatly reduced. These results, taken together with the behavioral work of D. Sanderson et al. [Sanderson, D., Good, M. A., Skelton, K., Sprengel, R., Seeburg, P. H., Nicholas, J., et al. Enhanced long-term and impaired short-term spatial memory in GluA1 AMPA receptor subunit knockout mice: Evidence for a dual-process memory model. Learning and Memory, 2009], provide genetic evidence that STP is a likely mechanism of STM.
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Weak repetitive synaptic stimulation can elicit an NMDA-dependent decaying potentiation referred to as short-term potentiation (STP).
“For instance, weak repetitive synaptic stimulation can elicit an NMDA-dependent decaying potentiation referred to as short-term potentiation (STP) (99–101).”
From Synaptic memory and CaMKII (2023) · cites this paper as [100]
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- Authors
- Erickson, M. A., Maramara, L. A., & Lisman, J.
- Affiliations
- Brandeis University (US)
- ORCID
- Lisman, John
- Venue
- Journal of Cognitive Neuroscience
- Publisher
- MIT Press
- Published
- 2010-11-01
- Volume
- 22
- Issue
- 11
- Pages
- 2530-2540
- ISSN
- 0898-929X (ISSN-L)
- 1530-8898
- PMC
- PMC3195522
- OpenAlex
- W2151112243
- Cited by
- 137
- References
- 5
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 13 · 2023: 8 · 2022: 8 · 2021: 7 · 2020: 7 · 2019: 9 · 2018: 8 · 2017: 14 · 2016: 6 · 2015: 12 · 2014: 9 · 2013: 11 · 2012: 6
- FWCI
- 2.36
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Cognitive Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (R01NS027337, R01 NS27337)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- short-term potentiation, short-term memory, GluR1, AMPA receptors, NMDA receptor, synaptic plasticity, synaptic depression, memory mechanisms
- MeSH terms
- Action Potentials, Animals, Animals, Newborn, Behavior, Animal, Electric Stimulation, Hippocampus, Memory, Short-Term, Mice, Inbred C57BL, Neural Inhibition, Picrotoxin, Time Factors, 2-Amino-5-phosphonovalerate, Long-Term Potentiation, Receptors, AMPA, Mice, Knockout, Patch-Clamp Techniques, Excitatory Amino Acid Antagonists, GABA Antagonists, Rats, Long-Evans, Mice, Rats, In Vitro Techniques
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