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Rodent audiogenic seizures (AS) (clonic-tonic convulsions in response to loud sound) epilepsy is the well-known phenomenon which isthe particular case of the refractory epilepsy. The morphological substrate of AS is well described, including brain stem structures withsubsequent involvement of midbrain and spinal motor neurons. The data on neurochemical traits in AS-prone rat strains (bredindependently) indicate the neurotransmitter misbalance in the background and as the response to AS. The data point as well to themultiple changes in numerous neurotransmitter systems which means probably that this type of brain pathology emerges during earlyontogeny. The polygenic determination of this trait was established several decades ago. Brain catecholamine (namely, gene cascadesof their release and inactivation) play the important role in AS expression, the brain noradrenergic (NA) machinery being among them.The data presented the first attempt to change the brain NA level by means of single injection of atomoxetine (15 and 30 mg/kg), thedrug which inhibits the NA reuptake. In male rats of highly AS-prone KM strain, atomoxetine decreased slightly the AS latency andintensity, while the similar treatment of 101/HY strain male mice (highly AS-prone) resulted in suppression of AS, and in control groupthe sound exposure resulted in death of 55% of animals (p<0.01). RussiaFunding: Supported by Russian Scientific Foundation, grant N 23-25-00042