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Introduction. Tetanus, also known as lockjaw, is a very dangerous infectious, acute, usually afebrile disease characterized by muscle spasms. The causative agent of the disease is bacteria Clostridium tetani. This bacteria produces a specific neurotoxin or tetanus toxin with two components: tetanospasmin and tetanolysin. Light chains of tetanospamine cleavage synaptobrevin, which in turn prevent release of the inhibitory neurotransmitter GABA into the synaptic cleft. The α - 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 normalize 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 dose of 5 mg/kg b.w.) and aminooxyacetic acid (at 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 hours following the application of tetanus toxin. It was found that haloperidol, given alone in a dose of 4 mg/kg, prolonged the survival time of mice with experimental tetanus, about 24.35 hour compared to the control group. Thus, application of haloperidol in this dose showed to be the only effective method. Additionally, combination of haloperidol with (-)-nuciferine slightly extend survival time, while combination with aminooxyacetic acid produced the best effect on the extension of this period (about 27.74 hour compared to the control group).
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