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Assessment of Memory Function in Pilocarpine-induced Epileptic Mice
Published on: June 4, 2020
Perirhinal cortex hyperexcitability in pilocarpine-treated epileptic rats
Ruba Benini1, Daniela Longo, Giuseppe Biagini
1Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, Montreal, Canada.
Hippocampus
|September 25, 2010
Summary
The perirhinal cortex (PC) in epilepsy exhibits synaptic hyperexcitability due to reduced inhibition. This study reveals functional network alterations in the epileptic PC, contributing to temporal lobe epilepsy.
Area of Science:
- Neuroscience
- Epileptology
- Cellular Electrophysiology
Background:
- The perirhinal cortex (PC) is implicated in seizure generation and spread due to its limbic system connections.
- Functional network alterations within an epileptic PC remain largely uncharacterized.
Purpose of the Study:
- To investigate functional changes in the perirhinal cortex (PC) network in an epilepsy model.
- To elucidate the role of the PC in the pathophysiology of temporal lobe epilepsy.
Main Methods:
- In vitro electrophysiology and immunohistochemistry were employed.
- Brain tissue from pilocarpine-treated epileptic rats and non-epileptic controls (NECs) was analyzed.
- Intrinsic neuronal properties, postsynaptic potentials, and epileptiform discharges were recorded and analyzed.
Main Results:
- Spontaneous and induced epileptiform discharges were observed in epileptic PC slices but not in controls.
- NMDA receptor antagonism reduced discharge duration; combined antagonism abolished them.
- Inhibitory postsynaptic potentials showed more depolarized reversal potentials in epileptic rats.
- Decreased potassium-chloride cotransporter 2 immunostaining and reduced parvalbumin, neuropeptide Y, and cholecystokinin-positive interneurons were noted in the epileptic PC.
Conclusions:
- Synaptic hyperexcitability in the epileptic PC is driven by attenuated inhibition.
- These findings highlight the critical role of perirhinal cortex networks in temporal lobe epilepsy pathogenesis.
