Deficient Hippocampal Long-Term Potentiation in α-Calcium-Calmodulin Kinase II Mutant Mice

Silva, Alcino J.; Stevens, Charles F.; Tonegawa, Susumu; Wang, Yanyan

doi:10.1126/science.1378648

Cited by 1,472Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsNeural dynamics and brain function

Deficient Hippocampal Long-Term Potentiation in α-Calcium-Calmodulin Kinase II Mutant Mice

Silva, Alcino J., Stevens, Charles F., Tonegawa, Susumu, Wang, Yanyan·1992·Science

DOI 10.1126/science.1378648

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Abstract

As a first step in a program to use genetically altered mice in the study of memory mechanisms, mutant mice were produced that do not express the alpha-calcium-calmodulin-dependent kinase II (alpha-CaMKII). The alpha-CaMKII is highly enriched in postsynaptic densities of hippocampus and neocortex and may be involved in the regulation of long-term potentiation (LTP). Such mutant mice exhibited mostly normal behaviors and presented no obvious neuroanatomical defects. Whole cell recordings reveal that postsynaptic mechanisms, including N-methyl-D-aspartate (NMDA) receptor function, are intact. Despite normal postsynaptic mechanisms, these mice are deficient in their ability to produce LTP and are therefore a suitable model for studying the relation between LTP and learning processes.

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The results with genetic deletion of CaMKIIα are variable, some showing roughly a 50% block and some showing a complete block.
“the results with the genetic deletion of CaMKIIα are more variable, some showing roughly a 50% block (87, 204–206) but some showing a complete block (121, 207, 208).”
From Synaptic memory and CaMKII (2023) · cites this paper as [204]
Most genetic deletion studies have failed to observe effects on baseline synaptic transmission.
“However, as mentioned above, most genetic deletion studies have failed to observe effects on baseline synaptic transmission (Refs. 43, 204, 205, but see Ref. 206).”
From Synaptic memory and CaMKII (2023) · cites this paper as [204]

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Authors: Silva, A. J., Stevens, C. F., Tonegawa, S., & Wang, Y.
Affiliations: Howard Hughes Medical Institute (US)
Salk Institute for Biological Studies (US)
ORCID: Silva, Alcino J.
Stevens, Charles F.
Tonegawa, Susumu
Venue: Science
Publisher: American Association for the Advancement of Science (AAAS)
Published: 1992-07-10
Volume: 257
Issue: 5067
Pages: 201-206
ISSN: 0036-8075 (ISSN-L)
1095-9203
DOI: 10.1126/science.1378648
OpenAlex: W2054975255
Cited by: 1,472
References: 1
Citations by year: 2026: 10 · 2025: 15 · 2024: 14 · 2023: 18 · 2022: 28 · 2021: 22 · 2020: 20 · 2019: 22 · 2018: 32 · 2017: 24 · 2016: 30 · 2015: 31 · 2014: 42 · 2013: 26 · 2012: 42
FWCI: 37.43
Type: journal article
Language: en
Open access: closed
Locations: Science (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r01ns012961-22)
National Institute of Neurological Disorders and Stroke (5 R01 NS 12961-17)
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: long-term potentiation, hippocampus, memory mechanisms, postsynaptic mechanisms, learning, genetically modified mice
MeSH terms: Animals, Behavior, Animal, Chromosome Mapping, DNA, Electrophysiology, Female, Hippocampus, Learning, Male, Mice, Inbred BALB C, Mice, Mutant Strains, Plasmids, Protein Kinases, RNA, Synapses, Transfection, Blotting, Southern, Blotting, Northern, Receptors, N-Methyl-D-Aspartate, Mutagenesis, Site-Directed, Calcium-Calmodulin-Dependent Protein Kinases, Mice

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Deficient Hippocampal Long-Term Potentiation in α-Calcium-Calmodulin Kinase II Mutant Mice

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