TEA elicits two distinct potentiations of synaptic transmission in the CA1 region of the hippocampal slice
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Extracellular application of tetraethylammonium (TEA) has been shown to elicit a prolonged synaptic potentiation in the CA1 region of the hippocampus that is unaffected by NMDA receptor antagonists, but is blocked by antagonists to voltage-dependent calcium channels (Aniksztejn and Ben-Ari, 1991; Huang and Malenka, 1993). In the present study the relation between TEA-induced potentiation and NMDA receptor- dependent long-term potentiation (LTP) was investigated in the CA1 region of the hippocampal slice using extracellular recordings and picrotoxin to block GABAA-mediated inhibition. Consistent with the finding of Huang and Malenka (1993), NMDA receptor-dependent LTP partially occluded the TEA-induced potentiation. However, this occlusion was abolished when the NMDA receptor antagonist D(-)-2-amino- 5-phosphonopentanoic acid (D-AP5) was present during the application of TEA, indicating one component of TEA-induced potentiation that is induced via NMDA receptor channels and another component that is distinct from NMDA receptor-dependent LTP. In the presence of antagonists to voltage-dependent calcium channels (nifedipine or nifedipine/flunarazine) application of TEA induced a potentiation that was largely occluded by NMDA receptor-dependent LTP. In common with NMDA receptor-dependent LTP, the TEA-induced potentiation, elicited in the presence of antagonists to voltage-dependent calcium channels, was associated with a symmetrical increase of the field EPSP. On the other hand, the TEA-induced potentiation elicited in the presence of D-AP5 produced an increase of the field EPSP that did not include the early part of the initial slope.(ABSTRACT TRUNCATED AT 250 WORDS)
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With intense induction protocols for LTP, a component of LTP requires the activation of VDCCs.
“with intense induction protocols for LTP a component of LTP requires the activation of VDCCs (49–51, 193, 196).”
From Synaptic memory and CaMKII (2023) · cites this paper as [51]
The Discussion (page unavailable) reports that high-frequency afferent activation produced prolonged potentiation that was much reduced by VDCC antagonists. But it says direct VDCC involvement in the potentiation seen after strong tetanization lacks evidence, and it does not establish that a component of tetanus-induced LTP requires VDCC activation. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAt CA1 excitatory synapses, both NMDAR-dependent and NMDAR-independent forms of LTP can coexist under certain conditions.
“There is even evidence that at CA1 excitatory synapses both NMDAR-dependent and NMDAR-independent forms of LTP can coexist under certain conditions (49–51).”
From Synaptic memory and CaMKII (2023) · cites this paper as [51]
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References 13 · Cited by 61
- Authors
- Hanse, E., & Gustafsson, B.
- Affiliations
- University of Gothenburg (SE)
- ORCID
- Hanse, E
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1994-08-01
- Volume
- 14
- Issue
- 8
- Pages
- 5028-5034
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6577179
- OpenAlex
- W1528821025
- Cited by
- 61
- References
- 13
- Citations by year
- 2026: 1 · 2023: 1 · 2022: 1 · 2019: 1 · 2015: 4 · 2014: 1 · 2013: 3
- FWCI
- 1.68
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Medical Research Council
- 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
- tetraethylammonium, synaptic potentiation, long-term potentiation, NMDA receptor, voltage-gated calcium channels, hippocampal CA1, field EPSP, D-AP5, nifedipine, picrotoxin, GABAA inhibition, synaptic plasticity
- MeSH terms
- Quaternary Ammonium Compounds, Animals, Calcium, Ganglionic Stimulants, Guinea Pigs, Hippocampus, Synaptic Transmission, Picrotoxin, Calcium Channels, 2-Amino-5-phosphonovalerate, Receptors, N-Methyl-D-Aspartate, Long-Term Potentiation
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