Krushinskii—Molodkina rats are genetically predisposed to the development of seizure activity in response to acoustic stimulation. These animals are a natural model to study the mechanisms of hereditary and audiogenic epilepsy. The main cause of these disorders is a deficiency of GABAergic transmission [3-5]. Biochemical and electrophysiological studies showed that this deficiency accompanies the increase in excitation transmission and is most pronounced in auditory structures, particularly in the relay structure (inferior colliculi of the quadrigeminal plate) [4-6]. The number of basket and GABA-containing neurons is maximum in this structure. The presence of a considerable number of these cells should contribute to the formation of the epileptic focus [5,7]. It was hypothesized that rats with genetic predisposition to audiogenic seizures differ from healthy animals in the structure of GABAAergic receptors in auditory structures [5,6]. It remains unknown whether seizure activity induced by epileptogenic acoustic stimulation can cause structural changes in auditory brain structures of these rats. Neuronal death is a typical morphological sign of various forms of epilepsy. Quantitative analysis of main cells (interneurons and GABA-containing cells) in the central nucleus of the inferior colliculi and anterior and posterior regions of the auditory cortex in Krushinskii—Molodkin rats was performed 1 month after audiogenic epileptic activity induced by acoustic stimulation.