Aberrant neuronal physiology in the basal nucleus of the amygdala in a model of chronic limbic epilepsy

Limbic epilepsy is a chronic condition associated with a broad zone of seiz ure onset and pathology. Studies have focused mainly on the hippocampus, bu t there are indications that changes occur in other regions of the limbic s ystem. This study used in vitro intracellular recording and histology to ex amine alterations to the physiology and anatomy of the basal nucleus of the amygdala in a rat model of chronic limbic epilepsy characterized by sponta neously recurring seizures. Epileptic pyramidal neuron responses evoked by stria terminalis stimulation revealed hyperexcitability characterized by mu ltiple action potential bursts and no evident inhibitory potentials. In con trast, no hyperexcitability was observed in amygdalar neurons from kindled (included as a control for seizure activity) or control rats. Blockade of i onotropic glutamate receptors unmasked inhibitory postsynaptic potentials i n epileptic pyramidal neurons. Control, kindled and epileptic inhibitory po tentials ware predominantly biphasic, with fast and slow components, but a few cells exhibited only the fast component (2/12 in controls, 0/3 in kindl ed, 3/10 in epileptic). Epileptic fast inhibitory potentials had a more rap id onset and shorter duration than control and kindled. Approximately 40% o f control neurons exhibited spontaneous inhibitory potentials; no spontaneo us inhibitory potentials were observed in neurons from kindled or epileptic rats. A preliminary histological examination revealed no gross alterations in the basal amygdala from epileptic animals. These results extend previous findings from this laboratory that hyperexcit ability is found in multiple epileptic limbic regions and may be secondary to multiple alterations in excitatory and inhibitory efficacy. Because ther e were no differences between control and kindled animals, the changes obse rved in the epileptic animals are unlikely to be secondary to recurrent sei zures. (C) 2000 IBRO. Published by Elsevier Science Ltd. All rights reserve d.