Feeding disturbances and EEG activity changes after amygdaloid kainate lesions in the rat

Kainic acid (KA), in various concentrations, was applied iontophoretically into the central nucleus of the amygdala. Microlesions with this cell specific neurotoxin caused body weight loss, hypo- or aphagia and hypo- or adipsia in a dose-dependent manner. EEG-examinations proved that even low doses of KA produced seizure activity; however, these epileptiform symptoms disappeared within the first 48 h after the operations. Thus, the lasting feeding disturbances produced by iontophoretic KA applications to the central nucleus of the amygdala (i.e., even these fine microlesions) were not related causally to the pathological EEG activity changes. Our findings, along with previous data, indicated that the body weight loss and feeding deficits were due to the KA-induced impairment of complex regulatory mechanisms.