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<a href="http://doi.org/10.1006/nlme.2001.4016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1006/nlme.2001.4016</a>
Pages
229–238
Issue
3
Volume
76
Dublin Core
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Title
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Depotentiation of vdccLTP requires NMDAR activation.
Publisher
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Neurobiology of learning and memory
Date
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2001
2001-11
Subject
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2-Amino-5-phosphonovalerate/pharmacology; Animals; Calcium Channel Blockers/*pharmacology; Calcium Channels/drug effects/*physiology; Electric Stimulation; Electrophysiology; Hippocampus/*physiology; Long-Evans; Long-Term Potentiation/*physiology; Male; N-Methyl-D-Aspartate/drug effects/*physiology; Nifedipine/*pharmacology; Organ Culture Techniques; Rats; Receptors; Synaptic Transmission/*physiology
Creator
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Morgan S L; Coussens C M; Teyler T J
Description
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Long-term potentiation is an enduring increase in synaptic efficacy following repeated stimulation of afferent fibers that is thought to underlie memory. In area CA1 of the hippocampus at least two forms of synaptic potentiation coexist at the same synapses; nmdaLTP and vdccLTP. NmdaLTP is induced by Ca2+ entry through NMDARs and is dependent on serine/threonine kinase activation, while vdccLTP is induced through Ca2+ entry through VDCCs and is dependent on tyrosine kinase activation. Depotentiation is a mechanism known to reverse nmdaLTP through phosphatase activation. The depotentiation of vdccLTP has not been previously investigated. We used hippocampal slices (area CA1) from male Long-Evans rats to induce vdccLTP with a 200-Hz tetanus in the presence of 50 microM APV. The 200-Hz tetanus resulted in a slowly developing vdccLTP that remained stable for at least 30 min. Thirty minutes after vdccLTP was induced, a low-frequency tetanus (3, 10, 20, 30, or 40 Hz) was applied in the presence of APV in an attempt to depotentiate vdccLTP. The 3- and 10-Hz low-frequency tetani resulted in no depotentiation. The 20- and 30-Hz tetani partially depotentiated vdccLTP (by approximately 13%), whereas the 40-Hz tetanus resulted in further potentiation. When APV was washed out prior to the 3-Hz low-frequency tetanus, the vdccLTP was completely depotentiated–presumably by NMDAR mechanisms. Our results indicate that vdccLTP is resistant to depotentiation under low-frequency stimulation conditions that readily depotentiate nmdaLTP. As tetanus frequencies are increased a small depotentiation is observed, suggesting that vdccLTP can be depotentiated to a small extent. When NMDARs are unblocked, vdccLTP can be completely depotentiated by a 3-Hz low-frequency tetanus, suggesting that vdccLTP can be depotentiated via activation of NMDAR mechanisms.
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<a href="http://doi.org/10.1006/nlme.2001.4016" target="_blank" rel="noreferrer noopener">10.1006/nlme.2001.4016</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2-Amino-5-phosphonovalerate/pharmacology
2001
Animals
Calcium Channel Blockers/*pharmacology
Calcium Channels/drug effects/*physiology
Coussens C M
Electric Stimulation
Electrophysiology
Hippocampus/*physiology
Long-Evans
Long-Term Potentiation/*physiology
Male
Morgan S L
N-Methyl-D-Aspartate/drug effects/*physiology
Neurobiology of learning and memory
Nifedipine/*pharmacology
Organ Culture Techniques
Rats
Receptors
Synaptic Transmission/*physiology
Teyler T J