The effect of haloperidol, aminooxyacetic acid and (-)-nuciferine on prolonging survival time of mice with tetanus

. Tetanus, also known as lockjaw, is a very dangerous, infectious, acute, usually afebrile disease characterised by muscle spasms. The causative agent of the disease is the bacterium Clostridium tetani. This pathogen produces a specific neurotoxin, termed tetanus toxin, with two components: tetanospasmin and tetanolysin. Light chains of tetanospasmin cleavage synaptobrevin, which in turn prevent release of the inhibitory neurotransmitter GABA into the synaptic cleft. The ?-motor neurons are, therefore, under no inhibitory control, as a result of which they undergo sustained excitatory discharge causing the characteristic motor spasms of tetanus. Materials and Methods. In this research, we attempted to normalise disorders caused by tetanus toxin by using haloperidol (at doses of 4, 5, 6, 7 and 8 mg/kg b.w.), alone and in combination with (-)-nuciferine (at a dose of 5 mg/kg b.w.) or aminooxyacetic acid (at a dose of 20 mg/kg b.w.). Experiments were conducted on albino mice. Experimental tetanus was induced by application of tetanus toxin. Results and Conclusions. Application of haloperidol (alone and in combination with (-)-nuciferine and aminooxyacetic acid) was carried out 24 h following the application of tetanus toxin. It was found that haloperidol, given alone in a dose of 4 mg/kg, prolonged the average survival time of mice with experimental tetanus by 24.35 h compared to the control animals. Additionally, the combination of haloperidol with (-)-nuciferine slightly, but non-significantly, extended survival time , while the combination of haloperidol with aminooxyacetic acid produced the best effect on extension of survival time (mice survived on average 27.74 h longer than control mice).