Ca2+ Entry via postsynaptic voltage-sensitive Ca2+ channels can transiently potentiate excitatory synaptic transmission in the hippocampus
Abstract
We have studied the role of Ca2+ entry via voltage-sensitive Ca2+ channels in long-term potentiation (LTP) in the CA1 region of the hippocampus. Repeated depolarizing pulses, in the presence of the NMDA receptor antagonist D-APV and without synaptic stimulation, resulted in a potentiation of excitatory postsynaptic potentials (EPSPs) or currents (EPSCs). This depolarization-induced potentiation was augmented in raised extracellular Ca2+ and was blocked by intracellular BAPTA, a Ca2+ chelator, or by nifedipine, a Ca2+ channel antagonist, indicating that the effect was mediated by Ca2+ entry via voltage-sensitive Ca2+ channels. Although the peak potentiation could be as large as 3-fold, the EPSP(C)s decayed back to baseline values within approximately 30 min. However, synaptic activation paired with depolarizing pulses in the presence of D-APV converted the transient potentiation into a sustained form. These results indicate that a rise in postsynaptic Ca2+ via voltage-sensitive Ca2+ channels can transiently potentiate synaptic transmission, but that another factor associated with synaptic transmission may be required for LTP.
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VPP does not occlude with LTP, strongly implying a mechanism distinct from LTP.
“VPP does not occlude with LTP (189, 192), strongly implying a mechanism distinct from LTP.”
From Synaptic memory and CaMKII (2023) · cites this paper as [189]
Voltage pulse potentiation (VPP) typically is transient, lasting no longer than 20 min.
“the potentiation typically is transient, lasting no longer than 20 min (Refs. 189–193, but see Refs. 194, 195).”
From Synaptic memory and CaMKII (2023) · cites this paper as [189]
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References 48 · Cited by 237
- Authors
- Kullmann, D. M., Perkei, D. J., Manabe, T., & Nicoll, R. A.
- Affiliations
- University of California, San Francisco (US)
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 1992-12
- Volume
- 9
- Issue
- 6
- Pages
- 1175-1183
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2024986310
- Cited by
- 237
- References
- 48
- Citations by year
- 2026: 2 · 2025: 2 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 2 · 2018: 3 · 2017: 7 · 2016: 3 · 2015: 1 · 2014: 1 · 2013: 8 · 2012: 4
- FWCI
- 11.03
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- voltage-gated calcium channels, calcium influx, long-term potentiation, excitatory postsynaptic potentials, hippocampal CA1, NMDA receptor, D-APV, extracellular calcium, BAPTA, nifedipine, paired-pulse stimulation, synaptic transmission
- MeSH terms
- Animals, Calcium, Egtazic Acid, Electric Stimulation, Evoked Potentials, Guinea Pigs, Hippocampus, Kinetics, Male, Synaptic Transmission, Nifedipine, Quinoxalines, Synapses, Time Factors, Calcium Channels, 2-Amino-5-phosphonovalerate, Receptors, N-Methyl-D-Aspartate, 6-Cyano-7-nitroquinoxaline-2,3-dione, In Vitro Techniques
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