The amygdala lesioning due to status epilepticus – Changes in mechanisms controlling chloride homeostasis

Objective: Amygdala has been demonstrated as one of the brain sites involved in the control of cardiorespiratory functioning. The structural and physiological alterations induced by epileptic activity are also present in the amygdala and reflect functional changes that may be directly associated with a sudden unexpected death. Seizures are always associated with neuronal damage and changes in the expression of cation-chloride cotransporters and Na/K pumps. In this study, the authors aimed to investigate if these changes are present in the amygdala after induction of status epilepticus with pilocarpine, which may be directly correlated with Sudden Unexpected Death in Epilepsy (SUDEP). Methods: Pilocarpine-treated wistar rats 60 days after Status Epilepticus (SE) were compared with control rats. Amygdala nuclei of brain slices immunostained for NKCC1, KCC2 and α1-Na+/K+-ATPase, were quantified by optical densitometry. Results: The amygdaloid complex of the animals submitted to SE had no significant difference in the NKCC1 immunoreactivity, but KCC2 immunoreactivity reduced drastically in the peri-somatic sites and in the dendritic-like processes. The α1-Na+/K+-ATPase peri-somatic immunoreactivity was intense in the rats submitted to pilocarpine SE when compared with control rats. The pilocarpine SE also promoted intense GFAP staining, specifically in the basolateral and baso-medial nuclei with astrogliosis and cellular debris deposition. Interpretation: The findings revealed that SE induces lesion changes in the expression of KCC2 and α1-Na+/K+-ATPase meaning intense change in the chloride regulation in the amygdaloid complex. These changes may contribute to cardiorespiratory dysfunction leading to SUDEP

Resposta eritropoética de ratos em diferentes graus de parasitemia por Trypanosoma evansi Erithropoietic response in Trypanosoma evansi infected rats with different parasitaemia intensity

O Trypanosoma evansi é um protozoário hemoflagelado que causa, em várias espécies, uma doença caracterizada por altos níveis de parasitemia, com rápido desenvolvimento de anemia. Este trabalho teve como objetivo investigar a relação entre o grau de parasitemia e a alteração na eritropoese de ratos (Rattus norvegicus) da linhagem Wistar infectados experimentalmente com T. evansi. Foram utilizados 42 ratos, dos quais 36 foram inoculados pela via intraperitoneal com 0,2ml de sangue, contendo 2,5 x 104 parasitas. Seis ratos não-inoculados foram utilizados como controles. Após inoculação, a parasitemia foi avaliada a cada 12h. Os grupos para análise foram estipulados de acordo com a média de tripanossomas em 10 campos homogêneos focados aleatoriamente, sendo: A, controle; B, animais que apresentaram um grau de parasitemia entre 1-10 tripanossomas/campo; C, ratos com 11-20 tripanossomas/campo; D, ratos com 21-30 tripanossomas/campo; E, ratos com 31-40 tripanossomas/campo; F, 41-50 tripanossomas/campo; e G, ratos com mais de 51 tripanossomas/campo. Quando os animais apresentaram o número de protozoários equivalente ao grupo, foram coletadas amostras de sangue para realização de hemograma e dosagem de ferro, e foi realizada citologia de medula óssea para avaliação da relação mielóide:eritróide. A análise estatística mostrou redução significativa das hemácias e do hematócrito a partir de 31 tripanossomas/campo (grupos E, F e G; P<0,005) e a redução de hemoglobina ocorreu a partir de 41 tripanossomas/campo (grupos F e G; P<0,005). A relação mielóide:eritróide foi reduzida de 0,7 para 0,6 a partir de 41 tripanossomas/campo (grupos F e G; P<0,005). Não foram detectadas variações na concentração de ferro. Os dados obtidos demonstraram que ratos com parasitemia acima de 31 tripanossomas por campo desenvolvem uma anemia aguda, com um aumento compensatório na atividade hematopoética.<br>Trypanosoma evansi is a flagellate protozoan that causes a disease characterized by high parasitemia and acute anemia in various species. This study was aimed at evaluating and establishing a relationship between different parasitemia levels and eritropoyesis in Wistar rats (Rattus norvegicus) experimentally infected by T. evansi. Forty two animals were used. In 36 animals parasites were inoculated by intraperitoneal blood injection of 0.2ml containing 2.5x104 parasites. Six non-inoculated animals were used as controls. Parasitemia was evaluated every 12 hours and the animals were allocated in groups according to parasitemia levels. Then they were classified according to average number of parasites in 10 random homogeneous fields, Group A: control (not-inoculated); B: rats with 1-10 trypanosomes/field; C: 11-20 trypanosomes/field; D: 21-30 trypanosomes/field; E: 31-40 trypanosomes/field; F: 41-50 trypanosomes/field; G: more then 51. Blood samples were taken when the animals reached the correspondent group number of parasites. Hemogram and iron levels were evaluated and a bone marrow cytology was performed to detect the myeloid:erythroid ratio. Statistical analysis showed a significant reduction on red blood cells count and hematocrit from group E on and also hemoglobin on groups F and G. The myeloid:erythroid ratio reduced from 0.7 to 0.6 on groups F and G (P<0.005). Iron levels alterations were not detected. These data showed that Wistar rats with parasitemia higher then 31 parasites per field have an acute anemia associated to a compensatory hematopoietic activity