Postsynaptic Calcium Is Sufficient for Potentiation of Hippocampal Synaptic Transmission
Abstract
Brief repetitive activation of excitatory synapses in the hippocampus leads to an increase in synaptic strength that lasts for many hours. This long-term potentiation (LTP) of synaptic transmission is the most compelling cellular model in the vertebrate brain for learning and memory. The critical role of postsynaptic calcium in triggering LTP has been directly examined using three types of experiment. First, nitr-5, a photolabile nitrobenzhydrol tetracarboxylate calcium chelator, which releases calcium in response to ultraviolet light, was used. Photolysis of nitr-5 injected into hippocampal CA1 pyramidal cells resulted in a large enhancement of synaptic transmission. Second, in agreement with previous results, buffering intracellular calcium at low concentrations blocked LTP. Third, depolarization of the postsynaptic membrane so that calcium entry is suppressed prevented LTP. Taken together, these results demonstrate that an increase in postsynaptic calcium is necessary to induce LTP and sufficient to potentiate synaptic transmission.
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When the intracellular electrode contained a Ca2+ chelator, no LTP occurred in the individual cell, while normal LTP was recorded from the field electrode.
“when the intracellular electrode contained a Ca2+ chelator no LTP occurred in the individual cell, while normal LTP was recorded from the field electrode”
From Synaptic memory and CaMKII (2023) · cites this paper as [177]
Photostimulation of cells loaded with the caged Ca2+ compound nitr-5 without depolarization enhanced responses.
“Photostimulation of cells loaded with the caged Ca2+ compound nitr-5 without depolarization of the cells enhanced responses (FIGURE 4C) (177).”
From Synaptic memory and CaMKII (2023) · cites this paper as [177]
All forms of hippocampal LTP have a common requirement for increased intracellular Ca2+ initiated either postsynaptically through NMDA receptors or presynaptically through voltage-sensitive Ca2+ channels.
“All forms of hippocampal LTP have a common requirement for increased intracellular C a 2ϩ initiated either postsynaptically through NMDA receptors or presynaptically through voltagesensitive C a 2ϩ channels (Kauer et al., 1988;Malenka et al., 1988;Nicoll et al., 1988).”
From Type I Adenylyl Cyclase Mutant Mice Have Impaired Mossy Fiber Long-Term Potentiation (1998) · cites this paper as Malenka et al., 1988
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- Authors
- Malenka, R. C., Kauer, J. A., Zucker, R. S., & Nicoll, R. A.
- Affiliations
- University of California, San Francisco (US)
- Department of Physiology and Anatomy, University of California, Berkdey, CA 94720.
- Venue
- Science
- Published
- 1988-10-07
- Volume
- 242
- Issue
- 4875
- Pages
- 81-84
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W1995484013
- Cited by
- 829
- References
- 1
- Citations by year
- 2026: 2 · 2025: 12 · 2024: 16 · 2023: 5 · 2022: 14 · 2021: 5 · 2020: 10 · 2019: 17 · 2018: 12 · 2017: 8 · 2016: 16 · 2015: 9 · 2014: 19 · 2013: 14 · 2012: 23
- FWCI
- 17.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (MH-38256, MH00437)
- National Institute of Neurological Disorders and Stroke (NS 24205)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- long-term potentiation, postsynaptic calcium, hippocampus, synaptic transmission, calcium chelators, photolysis, intracellular calcium buffering, postsynaptic depolarization, CA1 pyramidal neurons, learning and memory
- MeSH terms
- Animals, Calcium, Chelating Agents, Egtazic Acid, Evoked Potentials, Hippocampus, Kinetics, Synaptic Transmission, Photolysis, Pyramidal Tracts, Synapses, Rats, In Vitro Techniques
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