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Changes in neuronal excitability and synaptic function in a chronic model of temporal lobe epilepsy
C Bernard1, D P Marsden, H V Wheal
1Centre for Neuroscience, School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton, SO16 7PX, UK.
Neuroscience
|April 20, 2001
Summary
Excitatory postsynaptic potential/spike potentiation, a neuronal hyperexcitability marker, can be reversed in epilepsy models. This reversal suggests endogenous mechanisms can reduce neuronal excitability in chronic temporal lobe epilepsy.
Area of Science:
- Neuroscience
- Epilepsy Research
- Synaptic Physiology
Background:
- Excitatory postsynaptic potential/spike potentiation increases neuronal firing probability and is linked to epilepsy.
- This phenomenon has pro-epileptic consequences, contributing to hyperexcitability in brain tissue.
Purpose of the Study:
- To investigate the reversibility of excitatory postsynaptic potential/spike potentiation in a chronic epilepsy model.
- To explore the role of N-methyl-D-aspartate receptors and endogenous mechanisms in regulating this potentiation.
Main Methods:
- In vitro extracellular recordings in the CA1 area of kainic acid-lesioned rat hippocampus.
- Application of tetraethylammonium (a K+ channel blocker) to induce potentiation.
- Reversal of potentiation using low-frequency or tetanic stimuli.
Main Results:
- Tetraethylammonium induced excitatory postsynaptic potential/spike potentiation, which was reversible by electrical stimuli.
- A component of this potentiation and its reversal was independent of N-methyl-D-aspartate receptors.
- Tetraethylammonium also induced reversible N-methyl-D-aspartate receptor-mediated potentiation.
Conclusions:
- Excitatory postsynaptic potential/spike potentiation is reversible in epileptic tissue, even without synaptic plasticity.
- Endogenous regulatory mechanisms capable of decreasing cell excitability are present in epilepsy models.
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