| Abstrakt: |
It was established that mexidol (100 mg/kg, i.v.) in contrast to cytoflavin (1 ml/kg, i.v.) and reamberin (100 mg/kg, i.v.) produced analgesic effect in rabbits by raising pain threshold under electric stimulation of dental pulp. Mexidol (200 mg/kg, i.p.) also raised the nociceptive threshold of the same tail stimulation by in rats (vocalization test). Non-competitive antagonist of NMDA receptor complex, MK-801 (0.1 mg/kg, i.p.), and selective GABAA receptor antagonist bicuculline (1.5 mg/kg, i.p.) decrease the effect of mexidol. Therefore, the antinociceptive effect of mexidol in rats is mediated by the NMDA receptor complex and GABAA receptors. It was also found that mexidol (microiontophoretic application) produced inhibiting effect on spontaneous and evoked (caused by nociceptive electric stimulation of hind paw) activity of neurons (major part) of sensorimotor cortex and ventral posterior thalamic nucleus in rabbits. On the background of MK-801 and GABA blockers (bicuculline and picrotoxin), this action of mexidol was completely prevented or considerably decreased (by almost 80 and 60% of cells, respectively). Therefore, the effect of mexidol on these neurons is realized by inhibiting ion currents through NMDA receptor complex and via GABAA/benzodiazepine receptor complex. |
