The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Potentiated Transmission and Prevention of Further LTP by Increased CaMKII activity in Postsynaptic Hippocampal Slice Neurons
Abstract
Calcium-calmodulin-dependent protein kinase II (CaMKII) is a necessary component of the cellular machinery underlying learning and memory. Here, a constitutively active form of this enzyme, CaMKII(1-290), was introduced into neurons of hippocampal slices with a recombinant vaccinia virus to test the hypothesis that increased postsynaptic activity of this enzyme is sufficient to produce long-term synaptic potentiation (LTP), a prominent cellular model of learning and memory. Postsynaptic expression of CaMKII(1-290) increased CaMKII activity, enhanced synaptic transmission, and prevented more potentiation by an LTP-inducing protocol. These results, together with previous studies, suggest that postsynaptic CaMKII activity is necessary and sufficient to generate LTP.
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In the citing paper
“Calcium ions play a crucial role in initiating downstream signaling during long-term potentiation (LTP) and depression (LTD) and influx of calcium is both necessary and sufficient for structural synaptic plasticity (Pettit et al., 1994; Lledo et al., 1995; Otmakhov et al., 2004).”
From Barriers in the brain: resolving dendritic spine morphology and compartmentalization (2014) · cites this paper as Pettit et al., 1994
In the citing paper
“This is indeed the case (199, 209).”
From Synaptic memory and CaMKII (2023) · cites this paper as [209]
In the citing paper
“Expression of active CaMKII (121, 130–132, 209, 210, 212) or direct delivery into the cell via the recording electrode (199) has repeatedly revealed a roughly two- to threefold enhancement in the AMPAR EPSC but little change in the NMDAR EPSC (130–132).”
From Synaptic memory and CaMKII (2023) · cites this paper as [209]
In the citing paper
“This mutant induces LTP when introduced with a viral expression system (Pettit et al., 1994) or by direct injection into postsynaptic cells (Lledo et al., 1995).”
From Recruitment of the SNX17-Retriever recycling pathway regulates synaptic function and plasticity (2023) · cites this paper as Pettit et al., 1994
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Metadata
- Authors
- Pettit, D. L., Perlman, S., & Malinow, R.
- Affiliations
- University of Iowa (US)
- Venue
- Science
- Published
- 1994-12-16
- Volume
- 266
- Issue
- 5192
- Pages
- 1881-1885
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2076782463
- Cited by
- 329
- References
- 52
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 7 · 2023: 8 · 2022: 9 · 2021: 6 · 2020: 2 · 2019: 3 · 2018: 3 · 2017: 5 · 2016: 7 · 2015: 8 · 2014: 6 · 2013: 11 · 2012: 16
- FWCI
- 6.55
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- CaMKII, long-term potentiation, synaptic transmission, hippocampal neurons, postsynaptic activity, learning and memory, synaptic plasticity, recombinant vaccinia virus
- MeSH terms
- Animals, Cell Line, Genetic Vectors, Hippocampus, Membrane Potentials, Synaptic Transmission, Recombinant Proteins, Transfection, Vaccinia virus, 2-Amino-5-phosphonovalerate, Long-Term Potentiation, Calcium-Calmodulin-Dependent Protein Kinases, Pyramidal Cells, Patch-Clamp Techniques, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2, In Vitro Techniques
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