Abolition of Long-Term Stability of New Hippocampal Place Cell Maps by NMDA Receptor Blockade
Abstract
Hippocampal pyramidal cells are called place cells because each cell tends to fire only when the animal is in a particular part of the environment—the cell's firing field. Acute pharmacological blockade of N -methyl- d -aspartate (NMDA) glutamate receptors was used to investigate how NMDA-based synaptic plasticity participates in the formation and maintenance of the firing fields. The results suggest that the formation and short-term stability of firing fields in a new environment involve plasticity that is independent of NMDA receptor activation. By contrast, the long-term stabilization of newly established firing fields required normal NMDA receptor function and, therefore, may be related to other NMDA-dependent processes such as long-term potentiation and spatial learning.
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Pharmacological blockade of NMDARs prevents the stabilization of new place fields.
“However, pharmacological blockade of NMDARs prevents the stabilization of new place fields (418, 419)”
From Synaptic memory and CaMKII (2023) · cites this paper as [419]
Firing associations between dCA1 pyramidal cells reorganized to represent each environment.
“Additionally, we confirmed that firing associations between dCA1 pyramidal cells reorganized to represent each environment2,4,5,17(Supplementary Fig. 2a).”
From Dopaminergic neurons promote hippocampal reactivation and spatial memory persistence (2014) · cites this paper as [4]
New representations formed during exploration of novel environments or learning of new goal locations are initially labile and require stabilization to persist as memories.
“However new representations, such as those formed during exploration of novel environments or learning of new goal locations, are initially labile and thus require stabilization to persist as memories4-6.”
From Dopaminergic neurons promote hippocampal reactivation and spatial memory persistence (2014) · cites this paper as [4]
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“However, pharmacological blockade of NMDARs prevents the stabilization of new place fi elds (418, 419), and the genetic deletion of GluN1 in the CA1 region of the hippocampus decreases the spatial speci fi city of place fi elds (420).”
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- Authors
- Kentros, C., Hargreaves, E., Hawkins, R. D., Kandel, E. R., Shapiro, M., & Muller, R. V.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Kentros, Clifford
- Muller, Robert V.
- Venue
- Science
- Published
- 1998-06-26
- Volume
- 280
- Issue
- 5372
- Pages
- 2121-2126
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W1991880858
- Cited by
- 484
- References
- 21
- Citations by year
- 2026: 4 · 2025: 13 · 2024: 17 · 2023: 8 · 2022: 18 · 2021: 16 · 2020: 16 · 2019: 14 · 2018: 21 · 2017: 17 · 2016: 11 · 2015: 18 · 2014: 23 · 2013: 16 · 2012: 21
- FWCI
- 12.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Public Health Service (R01 45923, R01 20686)
- National Institute on Aging (T32 AGO 00189)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- place cells, hippocampus, NMDA receptor blockade, synaptic plasticity, firing fields, spatial learning, long-term potentiation, map formation, glutamate receptors
- MeSH terms
- Animals, Brain Mapping, Evoked Potentials, Hippocampus, Male, Memory, Neuronal Plasticity, Piperazines, Space Perception, Time Factors, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation, Pyramidal Cells, Excitatory Amino Acid Antagonists, Rats
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