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Text
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<a href="http://doi.org/10.1016/s0006-8993(01)02913-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/s0006-8993(01)02913-4</a>
Pages
90–96
Issue
1
Volume
917
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Title
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Epileptic-like activity induces multiple forms of plasticity in hippocampal area CA1.
Publisher
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Brain research
Date
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2001
2001-10
Subject
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*Neuronal Plasticity; Animals; Calcium Channels; Electrophysiology; Epilepsy/chemically induced/*physiopathology; Hippocampus/*physiopathology; Ion Channels/physiology; L-Type/physiology; Long-Evans; Long-Term Potentiation/physiology; N-Methyl-D-Aspartate/metabolism; Potassium Chloride; Rats; Receptors; Synapses/physiology
Creator
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Morgan S L; Teyler T J
Description
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Mesial temporal lobe epilepsy is a relatively common form of epilepsy that afflicts many thousands of people. It has been suggested that the development of primary and secondary foci may involve mechanisms similar to long-term potentiation (LTP). In vitro seizure models typically involve an increase in spontaneous asynchronous bursting activity (epileptiform activity) induced either by increasing excitation or decreasing inhibition. Previous experiments have indicated that these models often generate bursting activity that closely resembles epileptic activity. LTP is often observed following epileptiform activity. In area CA1 of the hippocampus two forms of LTP that are dependent on the activation of either the L-type voltage dependent calcium channel (vdccLTP) or the N-methyl-D-aspartate receptor/channel (nmdaLTP) have been described. It is unclear from previous experiments which type of LTP results from epileptiform activity. Recent evidence indicates that nmdaLTP is most likely a short-term type of plasticity while vdccLTP may be a long-lasting form of synaptic plasticity. Given the characteristics of vdccLTP it is a likely candidate mechanism to underlie the development and formation of secondary seizure foci. We have therefore tested the ability of epileptiform activity induced by elevated potassium chloride to induce multiple forms of LTP in area CA1 of the rat hippocampus. Elevation of extracellular potassium chloride resulted in spontaneous asynchronous bursting. The net result of the spontaneous asynchronous bursting was to induce a compoundLTP consisting of nmdaLTP and vdccLTP components.
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<a href="http://doi.org/10.1016/s0006-8993(01)02913-4" target="_blank" rel="noreferrer noopener">10.1016/s0006-8993(01)02913-4</a>
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*Neuronal Plasticity
2001
Animals
Brain research
Calcium Channels
Electrophysiology
Epilepsy/chemically induced/*physiopathology
Hippocampus/*physiopathology
Ion Channels/physiology
L-Type/physiology
Long-Evans
Long-Term Potentiation/physiology
Morgan S L
N-Methyl-D-Aspartate/metabolism
Potassium Chloride
Rats
Receptors
Synapses/physiology
Teyler T J