Tauber Simone C, Bunkowski Stephanie, Ebert Sandra, Schulz Daniela, Kellert Benedikt, Nau Roland, Gerber Joachim
Department of Neurology, Georg-August-University, Göttingen, Germany.
J Neurosci Res. 2009 Jun;87(8):1877-83. doi: 10.1002/jnr.22010.
An increase in adult neurogenesis was observed after exposure to enriched environment (EE) and during reconvalescence from experimental pneumococcal meningitis. This study investigated neurogenesis and spatial learning performance 5 weeks after bacterial meningitis and exposure to EE. C57BL/6 mice were infected by intracerebral injection of Streptococcus pneumoniae and treated with ceftriaxone for 5 days. Forty-eight hours after infection, one group (n = 22) was exposed to EE and the other group (n = 23) housed under standard conditions. Another set of mice was kept under either enriched (n = 16) or standard (n = 15) conditions without bacterial meningitis. Five weeks later, the Morris water maze was performed, and neurogenesis was evaluated by means of immunohistochemistry. Mice housed in EE without prior bacterial infection displayed both increased neurogenesis and improved water maze performance in comparison with uninfected control animals. Bacterial meningitis stimulated neurogenesis in the granular cell layer of the dentate gyrus: with standard housing conditions, we observed a higher density of BrdU-immunolabeled and TUC-4-expressing cells 5 weeks after induction of bacterial meningitis than in the noninfected control group. EE did not further increase progenitor cell proliferation and neuronal differentiation in the subgranular cell layer of the dentate gyrus after bacterial meningitis in comparison with infected mice housed under standard conditions. Moreover, the Morris water maze showed no significant differences between survivors of meningitis exposed to EE and animals kept in standard housing. In summary, exposure to EE after pneumococcal meningitis did not further increase meningitis-induced neurogenesis or improve spatial learning.
在暴露于丰富环境(EE)后以及实验性肺炎球菌脑膜炎康复期间,观察到成年神经发生增加。本研究调查了细菌性脑膜炎和暴露于EE 5周后的神经发生和空间学习表现。通过脑内注射肺炎链球菌感染C57BL/6小鼠,并用头孢曲松治疗5天。感染后48小时,一组(n = 22)暴露于EE,另一组(n = 23)饲养在标准条件下。另一组小鼠在没有细菌性脑膜炎的情况下饲养在丰富(n = 16)或标准(n = 15)条件下。5周后,进行莫里斯水迷宫实验,并通过免疫组织化学评估神经发生。与未感染的对照动物相比,饲养在EE中且无先前细菌感染的小鼠表现出神经发生增加和水迷宫表现改善。细菌性脑膜炎刺激了齿状回颗粒细胞层的神经发生:在标准饲养条件下,我们观察到细菌性脑膜炎诱导5周后,BrdU免疫标记和表达TUC-4的细胞密度高于未感染对照组。与饲养在标准条件下的感染小鼠相比,EE在细菌性脑膜炎后并未进一步增加齿状回颗粒下层祖细胞增殖和神经元分化。此外,莫里斯水迷宫实验显示,暴露于EE的脑膜炎幸存者与饲养在标准环境中的动物之间没有显著差异。总之,肺炎球菌脑膜炎后暴露于EE并未进一步增加脑膜炎诱导的神经发生或改善空间学习。