Genetically determined predisposition to convulsions as the result of a generalized defect in the metabolism of catecholamines in the central nervous system.

The author compared the functional properties of the striatal system in KM rats sensitive to the convulsive effects of sound with those in Wistar rats, which are insensitive to these effects. It was shown that bulbocapnine (an antagonist of dopamine) administered to the Wistar rats at a dose of 40 mg/kg body weight caused catalepsy, depressed the motor cortex excitability, and raised the threshold of the generalized Jacksonian-type convulsions. The KM rats showed neither catalepsy nor a rise in the generalized convulsion threshold, and the depression of the motor cortex excitability in them was only slight. Examinations of the apomorphine-induced stereotypy (dose 1.0-10 mg/kg) showed that in the KM rats the sensitivity of the receptors to dopamine was changed. The hyperproduction of catecholamines in the striatum, the hypothalamus, and adrenals in the KM rats suggests that the predisposition to epileptiform states correlates with the generalized defect in the metabolism of catecholamines. It is suggested that the hypersensitivity of KM rats to epileptogenic effects is due to a deficiency (caused by an excess of dopamine) in the depressing function of the striatum.

[Modeling different regimes of bioelectrical activity in the brain in normal subjects and in "increased readiness" in a network of neuron-like elements]. / Modelirovanie razlichnykh rezhimov bioélektricheskoi aktivnosti mozga v norme i pri povyshennoi "sudorozhnoi gotovnosti" na seti iz neironopodobnykh élementov.

Desynchronous (low voltage fast activity), synchronous (high voltage slow waves) as well as convulsive brain activities were stimulated by a computer model of neuronal population. Network excitatory and inhibitory elements possessed fundamental dynamic properties of real neurones. Being independent both of the excitability of elements and of external influence efficacy, synchronous (desynchronous) network activity resulted from the increase (decrease) of the average power of "neuronal" interconnections which imitated mutual and recurrent excitation and inhibition. The inhibition efficacy being reduced as compared with excitation, synchronization of elements became intensified. As a consequence, the rhythmic activity amplitude increased and the appearance of self-sustained oscillations simulating convulsive activity was facilitated. The probable mechanism of EEG activation by virtue of the reduction of mutual and recurrent excitation and inhibition efficacy as well as the significance of inhibitory mechanism deficiency for epileptogenesis are discussed.

[Catecholamine levels in the striatum, hypothalamus, and adrenals of rats with genetic predisposition to epileptic seizures]. / Soderzhanie katekholaminov v striatume, gipotalamyse i nadpochechnikakh krys, geneticheski predraspolozhennykh k sudorozhnym pripadkam.

The content of catecholamines (CA) was studied in the basal ganglia, hypothalamus and adrenals of Krushinsky-Molodkina (KM) rats exhibiting the increased sensitivity to convulsants, and of non-audiogenic Wistar rats. It was found that in all the structures under test the content of CA was considerably higher in KM than in Wistar rats. At the same time the concentration of dopamine in the basal ganglia and hypothalamus was far greater than that of the subsequent reaction products (noradrenaline, homovanillic and dioxyphenyl acetic acids), and the concentration of dopamine in the adrenals exceeded that of noradrenaline and adrenaline. Excess dopamine in the basal ganglia seems likely to be the reason for the failure of caudate nucleus inhibitory function in KM rats, thereby contributing to the increased sensitivity of the animals to convulsants. The relationship between the sensitivity to stressors and the initial level of CA metabolism is discussed.

[Genetically determined predisposition to convulsive seizures as a result of a generalized defect in catecholamine metabolism in the central nervous system]. / Geneticheski determinirovannaia predraspolozhennost' k sudorozhnym pripadkam kak sledstvie generalizovannogo defekta metabolizma katekholaminov v tsentral'noi nervnoi sisteme.

The author compared the functional properties of the strial system in KM rats sensitive to the convulsive effects of sound and in Wistar rats which are insensitive to those effects. It was shown that bulbocapnine (an antagonist of dopamine) administered to the Wistar rats in a dose of 40 mg/kg body weight caused catalepsy, depressed the motor cortex excitability and raised the threshold of the generalized Jacksonian-type convulsions. The KM rats showed neither catalepsy, nor the rise of the generalized convulsion threshold, and the depression of the motor cortex excitability in them was but slight. Examinations of the apomorphine-induced stereotypy (dose 1.0 to 10 mg/kg) showed that in the KM rats the sensitivity of the receptors to dopamine was changed. The hyperproduction of catecholamines in the striatum, the hypothalamus, and the adrenals in the KM rats suggests that the predisposition to epileptimorph states correlates with a generalized defect in the metabolism of catecholamines. It is supposed that the hypersensitivity of the KM rats to epileptogenic effects is due to a deficit (caused by the excess of dopamine) of striatum depressing function.