Mechanisms of Potentiation by Calcium-Calmodulin Kinase II of Postsynaptic Sensitivity in Rat Hippocampal CA1 Neurons
Abstract
Mechanisms of potentiation by calcium-calmodulin kinase II of postsynaptic sensitivity in rat hippocampal CA1 neurons. J. Neurophysiol. 78: 2682-2692, 1997. Preactivated recombinant alpha-calcium-calmodulin dependent multifunctional protein kinase II (CaMKII*) was perfused internally into CA1 hippocampal slice neurons to test the effect on synaptic transmission and responses to exogenous application of glutamate analogues. After measurement of baseline transmission, internal perfusion of CaMKII* increased synaptic strength in rat hippocampal neurons and diminished the fraction of synaptic failures. After measurement of baseline responses to applied transmitter, CaMKII* perfusion potentiated responses to kainate but not responses to N-methyl--aspartate. Internal perfusion of CaMKII*potentiated the maximal effect of kainate. Potentiation by CaMKII* did not change the time course of responses to kainate, whereas increasing response size by pharmacologically manipulating desensitization or deactivation rate constants significantly altered the time course of responses. Nonstationary fluctuation analysis of responses to kainate showed a decrease in the coefficient of variation after potentiation by CaMKII*. These data support the hypothesis that CaMKII increases postsynaptic responsiveness by increasing the available number of active alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid/kainate channels and suggests that a similar process may occur during the expression of long-…
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Overexpression of constitutively active CaMKII has little effect on synaptic NMDAR responses.
“overexpression of constitutively active CaMKII has little effect on synaptic NMDAR responses (130–132).”
From Synaptic memory and CaMKII (2023) · cites this paper as [132]
Expression of active CaMKII or direct delivery into the cell via the recording electrode has repeatedly revealed a roughly two- to threefold enhancement in the AMPAR EPSC but little change in the NMDAR EPSC.
“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 [132]
The number of NMDARs does not change during LTP, since constitutively active CaMKII does not affect the NMDAR EPSC and LTP is expressed primarily on the AMPAR.
“The number of NMDARs does not change, since constitutively active CaMKII does not affect the NMDAR EPSC (130–132) and LTP is expressed primarily on the AMPAR (19).”
From Synaptic memory and CaMKII (2023) · cites this paper as [132]
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References 78 · Cited by 47
- Authors
- Shirke, A. M., & Malinow, R.
- Affiliations
- University of Iowa (US)
- Cold Spring Harbor Laboratory (US)
- ORCID
- Malinow, Roberto
- Venue
- Journal of Neurophysiology
- Publisher
- American Physiological Society
- Published
- 1997-11-01
- Volume
- 78
- Issue
- 5
- Pages
- 2682-2692
- ISSN
- 0022-3077 (ISSN-L)
- 1522-1598
- OpenAlex
- W337872833
- Cited by
- 47
- References
- 78
- Citations by year
- 2024: 2 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 1 · 2018: 1 · 2016: 2 · 2015: 1 · 2012: 4
- FWCI
- 1.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurophysiology (publishedVersion)
- PubMed (publishedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Funders
- National Institutes of Health (5f31mh010524-02)
- National Institute of Mental Health (5 F31 MH-10524-02)
- 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 › Ion channel regulation and function
- Keywords
- calcium/calmodulin-dependent protein kinase II, postsynaptic potentiation, CA1 pyramidal neurons, synaptic transmission, kainate receptors, AMPA receptor desensitization, synaptic failure, long-term potentiation, glutamate analogues, synaptic plasticity
- MeSH terms
- Animals, Drug Synergism, Electric Stimulation, Hippocampus, Kainic Acid, Models, Neurological, Synaptic Transmission, Perfusion, Reaction Time, Recombinant Proteins, Synapses, Artifacts, Rats, Sprague-Dawley, Calcium-Calmodulin-Dependent Protein Kinases, Pyramidal Cells, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2, In Vitro Techniques
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