Introduction. Anticonvulsant drugs act on different molecular targets, selectively changing the excitability of neurons in such a way as to block the activity that leads to seizures without disrupting the normal activity required for the transmission of signals between neurons. The main mechanisms of reducing the excitability of neurons of the epielliptogenic focus are either inhibition of neuron activation or stimulation of inhibitory neurons. In general, these effects can be reduced to three main pharmaconeurophysiological mechanisms: enhancement of GABA or glycine transmission, reduction of excitatory (glutamate or aspartate) transmission, and nonspecific modulation of ion currents (sodium, calcium, and potassium channels). The most effective control of the tendency to convulsions is achieved precisely through the activation of GABA-ergic mechanisms. Propoxazepam, 7-bromo-5-(o-chlorophenyl)-3-propoxy-1,2-dihydro-3H-1,4-benzodiazepin-2-one, in the models of nociceptive and neuropathic pain showed significant analgesic activity. Similar to gabapentin and pregabalin, which are wellknown anti-epileptic drugs used in general medical practice in the treatment of neuropathic pain, propoxazepam also has an anticonvulsant effect, which explains the analgesic component of the pharmacological spectrum. The aim of the study was to find out and determine the mechanism of anticonvulsant action of propoxazepam on experimental animals using a wide range of convulsant substances. Materials and methods. Experiments were performed on outbred white mice of both sexes weighing 20-22 g. The use of different seizures inducers (picrotoxin (PCT), penthylenetetrazole (PTZ), strychnine (STR), thiosemicarbazide (TSC), bemegride (BMG), 4-aminopyridine (4-AP), and maximal electroshock (MES) allowed us to simulate different paroxyzmal manifestations and to suggest the propoxazepam mechanisms of antiseizure action. Results. The results indicate a high protective activity of propoxazepam based on the data of the dose-effect curves: PCT 1.67 ± 0.09, PTZ 0.9 ± 0.04, STR 14.24 ± 0.47, MES 0.57 ± 0.23, TSC 0.18 ± 0.09, 4-AP 37.3 ± 7.9 mg/kg. Depending on the type of сhemo convulsant, the protective dose of propoxazepam is significantly different (from 0.32 mg/kg for TSC up to 80 mg/kg for 4-AP), indicating a different degree of interaction with biotargets. Obviously, propoxazepam is more effective on the GABA-ergic dysfunction models, what is proved by a rise of the myoclonic component repre sentation in the seizures structrure with the simultaneous decrease of the tonic component. We have to mention that, on the BMG-induced seizures model, the relative quantity of the myoclonic component is only 32 %. This suggests the comparatively separate influence of benzdiazepine- and barbiturate-allosteric centers control. MES-induced seizures blocking demands the strong and steady cells hyperpolarization. Thus, the propoxazepam efficiency in this model is not very high. Moreover, even the relatively high doses (20 mg/kg) don't suppress the tonic component (68 %) possessing nevertheless, the protective action. The attention is attracted by the fact that in the model of 4-AP-induced seizures, propoxazepam not only shares the negligible effect (94 % of protective action is reached at a dose of 80 mg/kg), but also unusually redistributes the myoclonic and tonic components (reducing the firs and increasing the second component). Such peculiarities in the anticonvulsant action can be explained from the position of potassium ion channels functioning, which are inhibited by 4-AP. It is known that their activation leads to the membrane repolarization after the action potential development (participation in the potential restoring). Conclusion. Paying attention to such an «antiepileptic» effect, it is possible to suggest the division of propoxazepam and 4-AM actions -- first one acts predominantly on postsynaptic GABAA-receptors, causing the cell hyperpolarization, while the second interferes both pre- and postsynaptic potassium channels of the cell. Obviously, such an influence leads not only to the hyperpolarization efficiency reducing, but also increases the cell refractory period. Be cause of it, even the high doses of propoxazepam doesn′t share the 100 % efficiency in this model. [ABSTRACT FROM AUTHOR]