Detalhes bibliográficos
| Ano de defesa: |
2018 |
| Autor(a) principal: |
Müller, Pricila Tolio |
| Orientador(a): |
Boeck, Carina Rodrigues |
| Banca de defesa: |
Silva, Rosane Souza da,
Schuch, Natielen Jacques |
| Tipo de documento: |
Dissertação
|
| Tipo de acesso: |
Acesso aberto |
| Idioma: |
por |
| Instituição de defesa: |
Universidade Franciscana
|
| Programa de Pós-Graduação: |
Mestrado em Ciências da Saúde e da Vida
|
| Departamento: |
Ciências da Saúde e da Vida
|
| País: |
Brasil
|
| Palavras-chave em Português: |
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| Palavras-chave em Inglês: |
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| Área do conhecimento CNPq: |
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| Link de acesso: |
http://www.tede.universidadefranciscana.edu.br:8080/handle/UFN-BDTD/610
|
Resumo: |
Epilepsy is characterized by a cerebral disorder with interruptions, recurrent and unpredictable of normal brain function. Glutamate is the major excitatory neurotransmitter in the brain and is involved in the mechanism of status epilepticus - a prolonged and self-sustaining seizure. The drug N-methyl-D-aspartate (NMDA) is a synthetic excitotoxin that acts as a specific agonist for the NMDA receptor subtype of glutamate. Pre- and post-conditioning strategies provide a proposal for molecular mechanisms responsible for endogenous neuronal protection. The aim of the study is evaluating the effect of NMDA in different doses against damage following status epilepticus induced by pilocarpine in animal model of epilepsy. For this purpose, 210 adult male mice (60 days, 30-40 g) Swiss albino were treated intraperitoneally with pilocarpine (100 mg/kg every 20 min up to a maximum of 300 mg/kg) evoking status epilepticus. All animals were exposed to behavioral tasks for motor evaluation (locomotion, balance, motor coordination) and memory, followed by evaluation of cellular viability at 30 days post-pilocarpine. The pilocarpine death in approximately 40% of the mice during 24 hours. Treatment with lower doses of NMDA (18 mg/kg) prolonged survival time without change the outcome. The other NMDA doses also had no significant effect on the number of deaths. The status epilepticus caused reduction of the locomotor activity of the mice, an effect reversed by treatment with NMDA 37 mg/kg. The pilocarpine group mice did not show expressive cognitive deficit during acquisition of memory, however reduced evocation. Cellular viability assessed 30 days after status epilepticus indicated damage by MTT test, but not by propidium iodide. Only the 18 mg/kg NMDA reduced damage. It is concluded that the dose 18 mg/kg NMDA induced neuroprotection in surviving animals. The cellular mechanisms of NMDA-induced tolerance remain unknown, but the present study reinforces the dual NMDA effect, since the same dose that increased the mortality rate was able to reduce cellular damage. |
