The persistent effects of maternal infection on the offspring's cognitive performance and rates of hippocampal neurogenesis

• Published in: Progress in neuro-psychopharmacology & biological psychiatry Vol. 44; pp. 279 - 289
• Main Authors: Jiang, Peifang, Zhu, Tao, Zhao, Wenting, Shen, Jue, Yu, Yonglin, Xu, Jialu, Chen, Xi, Yu, Huimin
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01.07.2013; Elsevier
• Subjects: Age Factors; Animals; Animals, Newborn; Bacterial Infections - complications; Biological and medical sciences; Bromodeoxyuridine; Cell Count; Cognition Disorders - etiology; Cognition Disorders - microbiology; Cognition Disorders - pathology; Cognitive performance; Escherichia coli; Exploratory Behavior - physiology; Female; Glial Fibrillary Acidic Protein - metabolism; Hippocampus - microbiology; Hippocampus - pathology; Intrauterine infection; Male; Maze Learning - physiology; Medical sciences; Neurogenesis; Neurogenesis - physiology; Neuropharmacology; Orientation; Pharmacology. Drug treatments; Phosphopyruvate Hydratase - metabolism; PI3K–Akt signaling pathway; Pregnancy; Prenatal Exposure Delayed Effects - physiopathology; Rats; DG; E; PVL; SGZ; CNS; Neurogenesis; P; Cognitive performance; PI3K–Akt signaling pathway; PI3K; SVZ; E. coli; NSC/NPC; PBS; DGC; MWM; BDNF; Akt; CP; PVDF; GFAP; TrkB; NeuN; Intrauterine infection; BrdU; Infection; Progeny; Signal transduction; Central nervous system; Cognitive ability; Akt protein kinase; Pl3K―Akt signaling pathway; Hippocampus; Encephalon
• ISSN: 0278-5846; 1878-4216
• DOI: 10.1016/j.pnpbp.2013.03.007

Accumulating evidence indicates that perinatal infection is a major cause of neonatal neurologic morbidity. Here we explored the effects of maternal infection on the offspring's cognitive performance and hippocampal neurogenesis. Pregnant rats were treated with Escherichia coli suspension and allowed to deliver. Proliferating cells in the hippocampus were examined at postnatal (P) 3, 7, 14, and 28days and neuronal survival/differentiation was assessed at P28. Additionally, we examined the expressions of BDNF, TrkB and Akt. The cognitive performance of the offspring was assessed by the Morris water maze test. We found that maternal infection significantly impaired the offspring's spatial learning ability and spatial memory, thus could delay the cognitive performance development. Maternal infection significantly increased the number of proliferating cells in the offspring's hippocampus at postnatal 3, 7 and 14days, accompanied by significantly increased expressions of BDNF, TrkB and p-Akt at postnatal 3 and 7days. On postnatal 28days, maternal infection did not significantly affect the neuronal and glial differentiation, nor any significant changes in the expression levels of BDNF and TrkB in the hippocampus. Our result suggests that the hippocampal neurogenesis level may increase during early postnatal period after maternal infection. Increase of BDNF/TrkB expression and Akt activity may be the contributing molecular mechanism. •Maternal infection can delay the offspring's cognitive performance development.•Hippocampus neurogenesis may be enhanced by intrauterine E. coli infection.•PI3K–Akt signaling pathway may be activated by intrauterine E. coli infection.