Abstract
In order to examine the hypothesis that dysfunction of GABAergic system in the amygdala is related to the development of amygdaloid seizure, an GABA antagonist, bicuculline methiodide, was injected into the amygda of rats. Chemitrodes for both micro-injection and EEG recording were implanted into the left basolateral amygdala. Two weeks after surgery, the animals received single intra-amygdaloid injection of a large dose of bicuculline (10nmol) or repeated (every fourth day) injections of a small dose of bicuculline (0.2or O.4nmol).
The results were as follows. 1) In rats given a large dose of bicuculline, single injection elicited repetitive partial motor seizures which continued for over 60min. Finally, the epileptiform seizure developed to clonic generalized convulsions. 2) In rats given a small dose of bicuculline, repeated injections caused a progressive seizure development which was comparable to that seen in electrical kindling. The animals finally showed clonic generalized convulsions by the application of 5. 3 injections. 3) Histological examination showed prominent neuronal loss in some brain areas such as the bilateral hippocampi and pyriform cortices in the animals that had received the large dose of bicuculline. On the other hand, no histological changes specific to the antagonist injection was detected in the animals that had repeatedly received the small dose of the agent.
The present experiment indicates that suppression of the GABAergic function in the amygdala causes epileptiform seizures and that chemical kidnling is readily induced by repeated injection of a small dose of bicuculline.
