Laboratório de Microbiologia Experimental and Instituto Nacional de Ciência e Tecnologia Translacional em Medicina, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
Brain Res Bull. 2013 Mar;92:56-9. doi: 10.1016/j.brainresbull.2012.05.014. Epub 2012 Jun 7.
Streptococcus agalactiae (GBS) is a major cause of severe morbidity and mortality in neonates and young infants, causing sepsis, pneumonia and meningitis. The survivors from this meningitis can suffer serious long-term neurological consequences, such as, seizures, hearing loss, learning and memory impairments. Neurotrophins, such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) control the neuronal cell death during the brain development and play an important role in neuronal differentiation, survival and growth of neurons. Neonate Wistar rats, received either 10μL of sterile saline as a placebo or an equivalent volume of GBS suspension at a concentration of 1×10(6)cfu/mL. Sixty days after induction of meningitis, the animals underwent behavioral tests, after were killed and the hippocampus and cortex were retired for analyze of the BDNF and NGF levels. In the open-field demonstrated no difference in motor, exploratory activity and habituation memory between the groups. The step-down inhibitory avoidance, when we evaluated the long-term memory at 24h after training session, we found that the meningitis group had a decrease in aversive memory when compared with the long-term memory test of the sham group. BDNF levels decreased in hippocampus and cortex; however the NGF levels decreased only in hippocampus. These findings suggest that the meningitis model could be a good research tool for the study of the biological mechanisms involved in the behavioral alterations secondary to GBS meningitis.
无乳链球菌（GBS）是导致新生儿和婴幼儿严重发病和死亡的主要原因，可引起败血症、肺炎和脑膜炎。患有这种脑膜炎的幸存者可能会遭受严重的长期神经后果，例如癫痫发作、听力损失、学习和记忆障碍。神经营养因子，如神经生长因子（NGF）和脑源性神经营养因子（BDNF），可控制大脑发育过程中的神经元细胞死亡，并在神经元分化、存活和生长中发挥重要作用。新生 Wistar 大鼠，分别接受 10μL 无菌生理盐水作为安慰剂或浓度为 1×10（6）cfu/mL 的 GBS 悬浮液的等效体积。脑膜炎诱导 60 天后，动物进行行为测试，然后处死，取出海马体和皮质，分析 BDNF 和 NGF 水平。在旷场实验中，各组间的运动、探索性活动和习惯化记忆无差异。在避暗实验中，当我们在训练后 24 小时评估长时记忆时，我们发现与假手术组的长时记忆测试相比，脑膜炎组的厌恶记忆下降。BDNF 水平在海马体和皮质中降低；然而，NGF 水平仅在海马体中降低。这些发现表明，脑膜炎模型可能是研究与 GBS 脑膜炎相关的行为改变的生物学机制的良好研究工具。
