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Changes in neuronal excitability and synaptic function in a chronic model of temporal lope epilepsy

Changes in neuronal excitability and synaptic function in a chronic model of temporal lope epilepsy
Changes in neuronal excitability and synaptic function in a chronic model of temporal lope epilepsy
Long-term potentiation and depression of glutamatergic synaptic responses are accompanied by an increased firing probability of neurons in response to a given excitatory input. This property, named excitatory postsynaptic potential/spike potentiation, has also been described in epileptic tissue and has pro-epileptic consequences. In this study, we show that excitatory postsynaptic potential/spike potentiation can be reversed in the kainic acid lesioned rat hippocampus, a chronic model of temporal lobe epilepsy. Simultaneous in vitro extracellular recordings in stratum radiatum and stratum pyramidale were performed in the CA1 area of the kainic acid lesioned rat hippocampal slices. Fifteen minutes, application of the K(+) channel blocker tetraethylammonium resulted in excitatory postsynaptic potential/spike potentiation (measured 90min after the start of the washout period) which could be reversed by subsequent low-frequency or tetanic stimuli. Excitatory postsynaptic potential/spike potentiation and its subsequent reversal by an electrical conditioning stimulus were found to have a N-methyl-D-aspartate receptor-independent component. Tetraethylammonium treatment also resulted in excitatory postsynaptic potential/spike potentiation of pharmacologically isolated N-methyl-D-aspartate receptor-mediated responses which could be reversed by subsequent low-frequency or tetanic stimuli. We conclude that excitatory postsynaptic potential/spike potentiation can be reversed in epileptic tissue, even in the absence of synaptic plasticity. These results suggest the presence of endogenous regulatory mechanisms which are able to decrease cell excitability.
long-term potentiation, long-term depression, hippocampus, CA1, potassium channels, temporal lobe epilepsy
0306-4522
17-26
Bernard, C.
97d5a08e-1d4d-4166-b6a8-44b9d2e9dc45
Marsden, D.P.
9d4a6408-cdd4-4f3b-b55b-60839d13e708
Wheal, H.V.
50ba5833-9920-407a-a48a-1fe917534b74
Bernard, C.
97d5a08e-1d4d-4166-b6a8-44b9d2e9dc45
Marsden, D.P.
9d4a6408-cdd4-4f3b-b55b-60839d13e708
Wheal, H.V.
50ba5833-9920-407a-a48a-1fe917534b74

Bernard, C., Marsden, D.P. and Wheal, H.V. (2001) Changes in neuronal excitability and synaptic function in a chronic model of temporal lope epilepsy. Neuroscience, 103 (1), 17-26. (doi:10.1016/S0306-4522(00)00524-8).

Record type: Article

Abstract

Long-term potentiation and depression of glutamatergic synaptic responses are accompanied by an increased firing probability of neurons in response to a given excitatory input. This property, named excitatory postsynaptic potential/spike potentiation, has also been described in epileptic tissue and has pro-epileptic consequences. In this study, we show that excitatory postsynaptic potential/spike potentiation can be reversed in the kainic acid lesioned rat hippocampus, a chronic model of temporal lobe epilepsy. Simultaneous in vitro extracellular recordings in stratum radiatum and stratum pyramidale were performed in the CA1 area of the kainic acid lesioned rat hippocampal slices. Fifteen minutes, application of the K(+) channel blocker tetraethylammonium resulted in excitatory postsynaptic potential/spike potentiation (measured 90min after the start of the washout period) which could be reversed by subsequent low-frequency or tetanic stimuli. Excitatory postsynaptic potential/spike potentiation and its subsequent reversal by an electrical conditioning stimulus were found to have a N-methyl-D-aspartate receptor-independent component. Tetraethylammonium treatment also resulted in excitatory postsynaptic potential/spike potentiation of pharmacologically isolated N-methyl-D-aspartate receptor-mediated responses which could be reversed by subsequent low-frequency or tetanic stimuli. We conclude that excitatory postsynaptic potential/spike potentiation can be reversed in epileptic tissue, even in the absence of synaptic plasticity. These results suggest the presence of endogenous regulatory mechanisms which are able to decrease cell excitability.

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Published date: 28 February 2001
Keywords: long-term potentiation, long-term depression, hippocampus, CA1, potassium channels, temporal lobe epilepsy
Organisations: Biological Sciences

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Local EPrints ID: 35543
URI: http://eprints.soton.ac.uk/id/eprint/35543
ISSN: 0306-4522
PURE UUID: f0921b1c-2530-40d0-a0f5-31bbfb8bf5f9

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Date deposited: 18 May 2006
Last modified: 08 Jan 2022 12:57

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Contributors

Author: C. Bernard
Author: D.P. Marsden
Author: H.V. Wheal

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