It is shown that the serotonin receptors 5-HTlc , 5-HT3, and 5-HT 4 and ~2-adrenergic receptors are involved in the regulation of audiogenic seizures in DBA/2 mice, and that the effects of these serotonin receptors on the duration and magnitude of convulsive activity are the opposite of those produced by ct2-adrenergic receptors.Key Words: audiogenic seizures; cyproheptadine; ketanserin; mianserin; yohimbine; zakopride Knowledge of how the susceptibility to audiogenic seizures correlates with the activity of neurotransmitter systems is essential for understanding the mechanisms by which these seizures are regulated [1]. Experiments have shown that DBA/2 mice, which are genetically predisposed to seizures, and C57B1 mice, which are resistant, also differ in the activity of the serotoninergic, noradrenergic, gamma-aminobutyric acid, and several other brain systems [3,4,13,14]. The DBA/2 brain has been found to have much lower levels of serotonin (5-HT) and norepinephrine (NE), fewer binding sites for 3H-prazosin (a ligand of c~l-adrenergic receptors) [2], and a lower affinity of these receptors [5] than the C57B1 brain. Moreover, the temporal cortex of DBA/2 mice is reported to have far fewer monoamine-containing synapses than that of mice not susceptible to audiogenic seizures [8].Our previous studies demonstrated the importance of a balance between the activities of the brain serotoninergie and noradrenergic systems for the regulation of behavior; in particular, the two systems were shown to interact in a reciprocal