Changes in neuronal excitability and synaptic function in a chronic model of temporal lobe 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...

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Bibliographic Details
Published in:	Neuroscience Vol. 103; no. 1; pp. 17 - 26
Main Authors:	Bernard, C., Marsden, D.P., Wheal, H.V.
Format:	Journal Article
Language:	English
Published:	Oxford Elsevier Ltd 2001 Elsevier
Subjects:	Action Potentials Animals Biological and medical sciences CA1 Chronic Disease Epilepsy, Temporal Lobe - physiopathology Excitatory Postsynaptic Potentials Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Hippocampus Kainic Acid long-term depression Long-Term Potentiation Medical sciences Nervous system (semeiology, syndromes) Neurology Potassium Channel Blockers potassium channels Rats Rats, Wistar Receptors, AMPA Receptors, N-Methyl-D-Aspartate temporal lobe epilepsy Tetraethylammonium KA, kainic acid temporal lobe epilepsy hippocampus long-term depression TLE, temporal lobe epilepsy LTD, long-term depression PS, population spike LTP, long-term potentiation TEA, tetraethylammonium ACSF, artificial cerebrospinal fluid D-APV, d(−)-2-amino-5-phosphonopentanoic acid EPSP, excitatory postsynaptic potential CA1 LFS, low-frequency stimulation AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate potassium channels GABA, gamma-amino butyric acid LTPK, long-term potentiation induced by TEA application EPSP/spike, excitatory postsynaptic potential/spike TS tetanic stimulation CNQX, 6-cyano-7-nitroquinoxaline-2,3-dione PSA, population spike amplitude NMDA, N-methyl- d-aspartate long-term potentiation Potentiation Animal model Nervous system diseases Rat Rodentia Central nervous system Complex partial epilepsy Excitability Ionic channel Long term Cerebral disorder Vertebrata Chronic Mammalia Synaptic transmission Central nervous system disease Synaptic depression Temporal lobe epilepsy Potassium Hippocampus Brain (vertebrata)
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Summary:	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 90 min 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.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0306-4522 1873-7544
DOI:	10.1016/S0306-4522(00)00524-8