SBNeC 2010
Resumo:J.225


Poster (Painel)
J.225BEHAVIORAL CHARACTERIZATION OF AUDIOGENIC KINDLING IN WISTAR RATS PRIMED WITH AMINOGLYCOSIDE OR NOISE.
Autores:Orfa Yineth Galvis-alonso (FAMERP - Faculdade de Medicina de São José do Rio Preto) ; Mariana Carvalho dos Santos Tavares (FAMERP - Faculdade de Medicina de São José do Rio Preto) ; Lílian Nogueira (FAMERP - Faculdade de Medicina de São José do Rio Preto) ; José Henrique Dias (FAMERP - Faculdade de Medicina de São José do Rio Preto) ; Jorge Mejia (FAMERP - Faculdade de Medicina de São José do Rio Preto)

Resumo

RATIONALE: Rats, genetically susceptible to audiogenic seizures, develop limbic seizures when audiogenic ones are elicited in a periodic and chronic protocol, which is known as audiogenic kindling (AuK). Kanamycin and noise, applied in priming protocols, induce susceptibility to audiogenic seizures. OBJECTIVE: In this work, we studied the generation and evolution of audiogenic seizures during chronic acoustic stimulation of rats primed with kanamycin, amikacin or noise. METHODS: Wistar male (M) and female (F) rats received one intraperitoneal daily injection from postnatal day (PND) 9 to 12 with the following doses (mg/kg/day) of amikacin: 100 (n = 1F / 2M), 200 (n = 2F / 1M), 300 (n = 4F / 5M), 600 (n = 5F / 4M), and 900 (n = 1F / 4M), or kanamycin: 100 (n = 9F / 11M). A third group was stimulated with a school bell sound 120 dB (n = 9F / 10M) or 125 dB (n = 10F / 10M) during 8 minutes on PND 14. Control groups received saline solution 0.9% (n= 10F / 16M) or no sound (n= 10F / 12M). After that, beginning on PND 30, rats were submitted to a 30-stimulus AuK protocol. Finally, 30 days after Auk last stimulus, rats were re-stimulated using three stimuli (one/day). RESULTS: 1) 5% of kanamycin-treated and control rats presented audiogenic seizures; 2) 41% from amikacin and 30% from noise-treated rats became susceptible to audiogenic seizures; 3) proportion of stimuli that induce seizures was 10% and 30% in susceptible amikacin and noise groups, respectively; 4) 38% and 100% from amikacin and noise susceptible rats, respectively, presented limbic seizures during the AuK; 5) only limbic seizures from noise group presented progression and generalization. CONCLUSION: Wistar-FAMERP rats seem to be a more resistant strain to audiogenic seizure priming by aminoglycoside and noise. Progression of limbic seizure severity occurs mainly when audiogenic seizure susceptibility is induced by noise priming. Genetic factors influence induction of audiogenic seizure susceptibility and neural plasticity induced by amikacin and noise priming.


Palavras-chave:  neural plasticity, epileptogenesis, limbic kindling, epileptic transference, acoustic priming