Hyperexcitability of the CA1 Hippocampal Region during Epileptogenesis

• Published in: Epilepsia (Copenhagen) 2007-01, Vol.48 (s5), p.131-139
• Main Authors: El‐Hassar, Lynda, Esclapez, Monique, Bernard, Christophe
• Format: Article
• Language: English
• Subjects: Action Potentials - physiology; Animals; Biological and medical sciences; Complex syndromes; Disease Models, Animal; Electric Stimulation; Electroconvulsive therapy; Electrodes, Implanted; Electrophysiology; Epilepsy; Epilepsy - chemically induced; Epilepsy - physiopathology; Excitatory Postsynaptic Potentials - physiology; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Hippocampus; Hippocampus - physiopathology; Male; Medical genetics; Medical sciences; Models, Neurological; Nervous system (semeiology, syndromes); Neural Pathways - physiology; Neurology; Neuronal Plasticity - physiology; Pilocarpine; Psychology. Psychoanalysis. Psychiatry; Psychopathology. Psychiatry; Rats; Rats, Wistar; Synaptic Transmission - physiology; Treatments
• ISSN: 0013-9580; 1528-1167
• DOI: 10.1111/j.1528-1167.2007.01301.x

Temporal Lobe Epilepsy (TLE) is often preceded by a latent (seizure‐free) period during which complex network reorganizations occur. In experimental epilepsy, network hyperexcitability is already present during the latent period, suggesting a modification of information processing. The purpose of this study was to assess the input/output relationship in the hippocampal CA1 region during epileptogenesis. Field recordings in strata pyramidale and radiatum were used to measure the output of CA1 pyramidal cells as a function of the synaptic inputs they receive following the stimulation of Shaffer collaterals in slices obtained from sham and pilocarpine‐treated animals during the latent and chronic periods. We show that there is a transient increase of the input and output field responses during the latent period as compared to sham and epileptic animals. The coupling between excitatory inputs and cell firing was also increased during the latent period. This increase persisted in epileptic animals, although to a lesser extent. We also confirm that paired‐pulse facilitation occurs before the chronic phase. The present data further support the view that hyperexcitability is present at an early stage of epileptogenesis. Network output is more facilitated during the latent than during the chronic period. Hyperexcitability may participate to epileptogenesis, but it is not sufficient in itself to produce seizures.