The results demonstrate and confirm the significant role of monoamine imbalance in the ictogenesis of Krushinsky–Molodkina rats with genetically determined audiogenic epilepsy and in the development of audiogenic kindling (AuK) in them. The experiments were carried out on rats of the Krushinsky–Molodkina (KM) line without sound stimulation (KM-background) and after the development of AuK (KM-AuK). The control group was rats of line “0”, in which convulsions in response to sound were completely absent. AuK was generated using 20-fold sound stimulation (120 dB). Neurochemical analysis was performed by HPLC/ED in the frontal cortex, hippocampus, hypothalamus, nucleus accumbens, and brainstem. It has been established that AuK in KM rats leads to the appearance of myoclonic and attenuation of stem convulsions, which is accompanied by a change in the functional activity of the noradrenergic and serotonergic systems of the brain. KM rats exhibiting tonic convulsions in the “background” have a low content of norepinephrine in the hippocampus and hypothalamus, and when audiogenic myoclonic convulsions develop, norepinephrine deficiency is observed in the frontal cortex. After the formation of AuK, the excessively intense serotonin metabolism revealed in KM slows down in the hippocampus, nucleus accumbens, and, especially, in the brainstem, and the serotonin deficiency in the striatum also disappears. The peculiarities of norepinephrine metabolism in KM rats before and after AuK emphasize the important role of the cortex in the development of myoclonic convulsions, and of the hippocampus and hypothalamus in the implementation of stem convulsions. Excessive functional activity of the serotonergic system, revealed in KM “background” rats, slows down in a number of brain structures during the production of AuK.