Postsynaptic Inhibitors of Calcium/Calmodulin-Dependent Protein Kinase Type II Block Induction But Not Maintenance of Pairing-Induced Long-Term Potentiation
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The role of postsynaptic kinases in the induction and maintenance of long-term potentiation (LTP) was studied in the CA1 region of the rat hippocampal slice. A peptide inhibitor for the catalytic domain of calcium/calmodulin-dependent protein kinase type II (CaM-kinase) was applied through a perfused patch pipette. The inhibitor completely blocked both the short-term potentiation and LTP induced by a pairing protocol. This indicates that the kinase or kinases affected by the peptide are downstream from depolarization in the LTP cascade. The ability to block LTP required that measures be taken to interfere with degradation of the peptide kinase inhibitor by endogenous proteases; either addition of protease inhibitors or modifications of the peptide itself greatly enhanced the effectiveness of the peptide. Protease inhibitors by themselves or control peptide did not block LTP induction. To study the effect of kinase inhibitor on LTP maintenance, we induced LTP in one pathway. Subsequent introduction of the kinase inhibitor blocked the induction of LTP in a second pathway, but it did not affect maintenance of LTP in the first. The implications for the role of kinases in LTP maintenance are discussed.
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Numerous studies using peptide inhibitors have confirmed the block of LTP.
“Numerous studies using peptide inhibitors have confirmed the block of LTP (200–203).”
From Synaptic memory and CaMKII (2023) · cites this paper as [200]
Pharmacological inhibition of CaMKII activity has generally been reported not to affect synaptic responses.
“In addition, pharmacological inhibition of CaMKII activity has generally been reported not to affect synaptic responses (198, 200–203, 357, 358).”
From Synaptic memory and CaMKII (2023) · cites this paper as [200]
Numerous previous studies have failed to reverse established LTP.
“However, numerous previous studies have failed to reverse established LTP (Refs. 198, 200–203, but see Ref. 357).”
From Synaptic memory and CaMKII (2023) · cites this paper as [200]
Concentrations of CaMKII inhibitors that block the induction of LTP failed to affect maintenance.
“Third, as discussed in sect. 8, concentrations of CaMKII inhibitors that block the induction of LTP failed to affect maintenance (Refs. 198, 200–203, but see Ref. 357).”
From Synaptic memory and CaMKII (2023) · cites this paper as [200]
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References 72 · Cited by 207
Research works printed but not linked: 3
- Barria A, Muller D, Griffith LC, Soderling TR (1997) Phosphorylation of AMPA-type glutamate receptors by C a 2ϩ /calmodulin-dependent protein kinase II during long-term potentiation. Science, in press.
- Malgaroli A, Malinow K , Schulman H, Tsien RW (1992) Persistent signaling and changes in presynaptic f unction in long-term potentia- tion. In: Interactions among cell signaling systems (Sato R, ed), pp 176 -191. Chichester, UK : Wiley.
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- Authors
- Otmakhov, N., Griffith, L. C., & Lisman, J. E.
- Affiliations
- Brandeis University (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1997-07-15
- Volume
- 17
- Issue
- 14
- Pages
- 5357-5365
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6793827
- OpenAlex
- W1802372728
- Cited by
- 207
- References
- 72
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 3 · 2019: 6 · 2018: 6 · 2017: 6 · 2016: 4 · 2015: 7 · 2014: 8 · 2013: 7 · 2012: 7
- FWCI
- 3.78
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- W. M. Keck Foundation
- National Institutes of Health
- National Institute of General Medical Sciences (R01GM054408)
- National Institute of Neurological Disorders and Stroke (R01NS027337, 2 RO1 NS-27337)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- long-term potentiation, calcium/calmodulin-dependent protein kinase II, CaMKII, LTP induction, LTP maintenance, protease degradation, protease inhibitors, hippocampal CA1, synaptic plasticity, short-term potentiation
- MeSH terms
- Animals, Enzyme Inhibitors, Hippocampus, Male, Synaptic Transmission, Protease Inhibitors, Long-Term Potentiation, Calcium-Calmodulin-Dependent Protein Kinases, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2
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