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Induction of Epileptiform Activity by Temperature Elevation in Hippocampal Slices from Young Rats: An In Vitro Model for Febrile Seizures?
Author(s) -
Tancredi V.,
D'Arcangelo G.,
Zona C.,
Siniscalchi A.,
Avoli M.
Publication year - 1992
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1992.tb02311.x
Subject(s) - orthodromic , hippocampal formation , chemistry , population , hippocampus , population spike , bicuculline , electrophysiology , stimulation , convulsants , convulsant , neuroscience , endocrinology , medicine , epilepsy , anesthesia , psychology , anticonvulsant , biochemistry , gabaa receptor , dentate gyrus , receptor , environmental health
Summary: Extracellular field potential recordings were performed in the CA1 subfield of hippocampal slices obtained from Wistar rats aged 2–38 days. When the brain tissue was maintained at 35°–36°C (values obtained in the tissue chamber well), single‐shock orthodromic stimuli elicited a response in the stratum pyramidale that consisted of a single population spike. In contrast, when the temperature in the well was increased to levels >38.2°C for periods of 5–15 min, the same type of stimuli elicited an epileptiform response characterized by a 250‐ to 600‐ms‐long, positive‐going field potential with superimposed, multiple, negative‐going population spikes. This potential resembled the epileptiform response recorded in the hippocampal slice in the presence of convulsants such as penicillin or bicuculline. Once the temperature was restored to control values (i.e., 35°–36°C) after induction of epileptiform activity, the abnormal response could be observed for 2 h. In some experiments (approximately one third of the successful trials), spontaneous epileptiform discharges appeared during and persisted after the increase in temperature. The ability of the hyperthermic period to induce epileptiform changes was age dependent: Epileptiform activity outlasting the period of temperature elevation was not observed in slices obtained from rats aged <4 days or >28 days. Our data show that epileptiform activity can be induced by a transient increase in temperature and that the age of the animals from which slices are obtained plays an important role in the appearance of this phenomenon. Both characteristics indicate that this in vitro model of epileptiform activity might represent an experimental preparation suitable for studying the cellular and pharmacologic mechanisms underlying febrile convulsions. Knowledge of these mechanisms might help in designing better strategies for therapeutic management of such seizures.