Abstract The kindling model of epilepsy is based on a permanent alteration in brain function resulting from repeated subconvulsant stimulation. Because these alterations may be neurochemical in nature, the role of serotonin (5-HT) in the development of amygdaloid-kindled seizures was studied using female rats. Concentrations of 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) were determined fluorometrically in the hypothalamus, amygdala, midbrain, and brain-stem regions. Amygdaloid kindling led to significant decreases of 5-HT and 5-HIAA in the midbrain region. The administration of 5-hydroxytryptophan (5-HTP), a 5-HT precursor, was found to retard the evolution of the kindling process and p-chlorophenylalanine ( p-CPA), a depletor of brain 5-HT, facilitated the development of amygdaloid kindled seizures. Both 5-HTP and p-CPA produced an increase in afterdischarge duration of full kindled seizures. The data suggest that serotonergic mechanisms may play a suppressive role in the development of amygdaloid-kindled seizures.