title: [On the mechanism of antimotion sickness effects of mexidol].
abstract: The path-clamp method used within the whole-cell configuration in experiments with convoluted medullar oblongata sections obtained from white mongrel male rats aged 13 to 17 days evidenced that 5 mV of mexidol caused 96 +/- 2% inhibition of the excitation postsynaptic current in neurons of the medial vestibular nucleus generated by the depolarization step of 10 mV (holding potential = -70 my). This means that the antimotion sickness effect of mexidol has its origin in the ion mechanisms with involvement of the glutamate- and GABAergic components, primarily inhibition of ion currents through channels of the NMDA-receptor complex.
authors.forename: V G
authors.initials: VG
authors.lastname: Motin
authors.forename: V V
authors.initials: VV
authors.lastname: Iasnetsov
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D008297:Male; D009041:Motion Sickness / Q000188:drug therapy* / Q000503:physiopathology*; D010847:Picolines / Q000008:administration & dosage*; D051381:Rats; D014726:Vestibular Nuclei / Q000187:drug effects* / Q000503:physiopathology*
chemical_list: D000975:Antioxidants; D010847:Picolines; C070020:emoxypine succinate