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Cited by 172Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsProtein Kinase Regulation and GTPase Signaling

Postsynaptic injection of Ca2+/CaM induces synaptic potentiation requiring CaMKII and PKC activity

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Wang, Jin-Hui, Kelly, Paul T.·1995·Neuron
DOI 10.1016/0896-6273(95)90048-9
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Abstract

CA2+-regulated protein kinases play critical roles in long-term potentiation (LTP). To understand the role of Ca2+/calmodulin (CaM) signaling pathways in synaptic transmission better, Ca2+/CaM was injected into hippocampal CA1 neurons. Ca2+/CaM induced significant potentiation of excitatory synaptic responses, which was blocked by coinjection of a CaM-binding peptide and was not induced by injections of Ca2+ or CaM alone. Reciprocal experiments demonstrated that Ca2+/CaM-induced synaptic potentiation and tetanus-induced LTP occluded one another. Pseudosubstrate inhibitors or high-affinity substrates of CaMKII or PKC blocked Ca2/CaM-induced potentiation, indicating the requirement of CaMKII and PKC activities in synaptic potentiation. We suggest that postsynaptic levels of free Ca2+/CaM is a rate limiting factor and that functional cross-talk between Ca2+/CaM and PKC pathways occurs during the induction of LTP.

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Crossref · 10.1016/0896-6273(95)90048-9

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2 of 2 references verified0 citation errors · 0 not checkable

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  • Loading cells with Ca2/CaM from the recording electrode caused a slowly developing enhancement that occluded LTP.

    “This caused a slowly developing enhancement that occluded LTP.”

    From Synaptic memory and CaMKII (2023) · cites this paper as [184]

  • Synapses expressing LTP are not enhanced by Ca2+/calmodulin.

    “synapses expressing LTP are not enhanced by Ca2+/calmodulin.”

    From Synaptic memory and CaMKII (2023) · cites this paper as [184]

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Authors
Wang, J.-H., & Kelly, P. T.
Venue
Neuron
Publisher
Elsevier BV
Published
1995-08
Volume
15
Issue
2
Pages
443-452
ISSN
0896-6273 (ISSN-L)
DOI
10.1016/0896-6273(95)90048-9
OpenAlex
W2022924617
Cited by
172
References
2
Citations by year
2026: 1 · 2025: 1 · 2024: 2 · 2023: 4 · 2022: 2 · 2021: 2 · 2020: 2 · 2019: 5 · 2018: 3 · 2017: 2 · 2016: 2 · 2015: 7 · 2014: 3 · 2013: 2 · 2012: 4
FWCI
4.53
Type
journal article
Language
en
Open access
Licence
Locations
  • Neuron (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01ns032470-08)
  • National Institute of Neurological Disorders and Stroke (NS-32470)
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
synaptic potentiation, long-term potentiation, CaMKII, protein kinase C, CA1 pyramidal neurons, tetanic stimulation, excitatory synaptic transmission
MeSH terms
Amino Acid Sequence, Animals, Calcium, Calmodulin, Calmodulin-Binding Proteins, Electric Stimulation, Male, Membrane Potentials, Molecular Sequence Data, Nerve Tissue Proteins, Peptide Fragments, Phosphorylation, Protein Kinase C, Protein Processing, Post-Translational, Signal Transduction, Rats, Sprague-Dawley, Long-Term Potentiation, Cyclic AMP-Dependent Protein Kinases, Calcium-Calmodulin-Dependent Protein Kinases, Patch-Clamp Techniques, Rats, Neurogranin, Calcium-Calmodulin-Dependent Protein Kinase Type 2

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