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Cited by 126Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsProtein Kinase Regulation and GTPase Signaling

The DOI matches its Crossref record; 70 of the 70 references it cites were found in a registry or an index.

Is Persistent Activity of Calcium/Calmodulin-Dependent Kinase Required for the Maintenance of LTP?

Chen, Huan-Xin, Otmakhov, Nikolai, Strack, Stefan, Colbran, Roger J., Lisman, John E.·2001·Journal of Neurophysiology
DOI 10.1152/jn.2001.85.4.1368
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Abstract

Calcium/calmodulin-dependent protein kinase II (CaMKII) is concentrated in the postsynaptic density (PSD) and plays an important role in the induction of long-term potentiation (LTP). Because this kinase is persistently activated after the induction, its activity could also be important for LTP maintenance. Experimental tests of this hypothesis, however, have given conflicting results. In this paper we further explore the role of postsynaptic CaMKII in induction and maintenance of LTP. Postsynaptic application of a CaMKII inhibitor [autocamtide-3 derived peptide inhibitor (AC3-I), 2 mM] blocked LTP induction but had no detectable affect on N-methyl-D-aspartate (NMDA)-mediated synaptic transmission, indicating that the primary function of CaMKII in LTP is downstream from NMDA channel function. We next explored various methodological factors that could account for conflicting results on the effect of CaMKII inhibitors on LTP maintenance. In contrast to our previous work, we now carried out experiments at higher temperature (33 degrees C), used slices from adult animals, and induced LTP using a tetanic stimulation. However, we still found that LTP maintenance was not affected by postsynaptic application of AC3-I. Furthermore the inhibitor did not block LTP maintenance under conditions designed to enhance the Ca(2+)-dependent activity of protein phosphatases 1 and 2B (elevated Ca(2+), calmodulin, and an inhibitor of protein kinase A). We also tested the possibility that CaMKII in…

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Research works printed but not linked: 2

  1. Malgaroli A, 1992, Ciba Found Symp, 164, 176
  2. Shenolikar S, 1991, Adv Second Messenger Phosphoprotein Res, 23, 1

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Metadata

Authors
Chen, H.-X., Otmakhov, N., Strack, S., Colbran, R. J., & Lisman, J. E.
Affiliations
  • Volen Center for Complex Systems, Brandeis University, Waltham, Massachusetts 02454; and
  • Brandeis University (US)
  • Vanderbilt University (US)
ORCID
Venue
Journal of Neurophysiology
Publisher
American Physiological Society
Published
2001-04-01
Volume
85
Issue
4
Pages
1368-1376
ISSN
  • 0022-3077 (ISSN-L)
  • 1522-1598
DOI
10.1152/jn.2001.85.4.1368
OpenAlex
W2316453747
Cited by
126
References
70
Citations by year
2025: 1 · 2024: 4 · 2023: 2 · 2022: 1 · 2021: 4 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 5 · 2016: 3 · 2015: 2 · 2014: 7 · 2013: 6 · 2012: 7
FWCI
2.31
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurophysiology (publishedVersion)
  • PubMed (publishedVersion)
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, LTP maintenance, postsynaptic density, CaMKII inhibitor, NMDA receptor, calcineurin, protein phosphatase 1, calmodulin, autophosphorylation, tetanic stimulation, temperature effects, synaptic plasticity
MeSH terms
Animals, Electric Conductivity, Electrophysiology, Enzyme Inhibitors, Male, Peptides, Synapses, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation, Calcium-Calmodulin-Dependent Protein Kinases, Rats, Long-Evans, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2

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