Schistosomiasis is a tropical disease caused by Schistosoma mansoni. His occurrence affects 110 million people worldwide. The deposition of eggs of the parasite may occur - in ectopic form – in the central nervous system (CNS) which leads to the formation of granulomas with consequent production of nerve growth factor (NGF). Since several studies have demonstrated the importance of NGF in the development of visual cortical pathways, our study aimed at evaluating the possible changes in the NGF concentratons in the visual system as well as the impact of this on the pyramidal cell morphology in two animal models. The change in concentration of the nerve growth factor as well as neuronal morphology were evaluated in suscetible and non-suscetible animals (mice and rats) to infection. We used 174 rats (Hooded Lister) and 135 albino mice bred and kept in cages and fed ad libitum. These animals were infected shortly after birth, with 50 cercariae. Seventy seven rats and 73 mice were inoculated with saline and constituted the control group of the study. The infection covered a period of 48 weeks . Samples of liver and visual cortex were removed, extracted and quantified with immunoassay kit (ChemiKineTM Nerve Growth Factor (NGF) Sandwich ELISA Kit - Chemicon International). For the morphometric analysis we used the pyramidal cells of the visual cortex layer IV marked by extracelular injection of biotinylated dextran (10,000 kDa). The results were expressed as mean ± standard deviation. We used Student t test to determine statistical differences between groups. The average value of NGF found in the visual cortex of rats infected was 39.2% higher than in the control group (infected: 400.9 ± 143.1 pg/ml, control: 288 ± 31.9 pg/mL, p < 0.0001). In liver samples, the increase was 28.9% higher in the infected group (infected: 340.9 ± 103.9 pg/mL, p < 0.01, control: 264.4 ± 38.6 pg/mL). No significant increase was detected within a week of infection. Among the mice group, the increase of NGF in the visual area was 94.1% (infected: 478.4 ± 284 pg/ml, p < 0.01; control: 246.5 ± 76.8 pg/ml). In the liver of these animals the increase was 138.7% (infected: 561.8 ± 260.7 pg/mL, p < 0.01, control: 301.3 ± 134.6 pg/mL). In mice group we found significant differences in dendritic parameters evaluated. The number of dendrites was 11.41% higher in the infected group than in the control (control: 25.28 ± 5.19; infected: 28.16 ± 7.45, p < 0.05). The total length of dendrites was also affected (control: 4916.52 ± 1492.65 μm; Infected: 5460.40 ± 1214.07 μm; p < 0.05), representing an increase of 11.06%. The total area of the dendritic receptive field was increased by 12.99% (control: 29.346,69 ± 11.298,62 μm2; Infected: 33.158,20 ± 7.758,31 μm2, p < 0.05) while the area had a somatic reduction of 13.61% (control: 119.38 ± 19.68 μm2; infected: 103.13 ± 24.69 μm2, p < 0.001). When we evaluated the effects of increased NGF in rats infected we did not observe significant differences in dendritic parameters analyzed, compared to the control group, except for an increase in the area of the neuronal body of approximately 21.18% (control: 132,20 ± 28.46 μm2; infected: 160.20 ± 31.63 μm2, p < 0.00001). This work showed that the reaction production of NGF in the CNS during infection with Schistosoma mansoni occurs in greater magnitude than permissible in the model in the model impermissible. We also demonstrated that in mice the effects on neuronal morphology is dramatically affected when the body is subjected to an increase in the concentration of NGF as a result of infection by Schistosoma mansoni. Given these data, studies evaluating the potential impact of visual effects and also in cell physiology caused by schistosomiasis infection becomes necessary to assess the actual damage caused by this pathological increase of nerve growth factor in the visual pathways of mammals.
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