title: Prenatal exposure to lipopolysaccharide results in cognitive deficits in age-increasing offspring rats.
abstract: Studies have suggested that maternal infection/inflammation maybe a major risk factor for neurodevelopmental brain damage. In the present study, we evaluated the effects of prenatal exposure to a low level of inflammatory stimulation lipopolysaccharide (LPS) repeatedly on spatial learning and memory performances in rat offspring's lifetime. Sixteen pregnant Sprague-Dawley rats were randomly divided into two groups. The rats in the LPS group were treated i.p. with LPS (0.79 mg/kg) at gestation day 8, 10 and 12; meanwhile the rats in the control group were treated with saline. After delivery, the rat offspring at 3- (young), 10- (adult) and 20-mon-old (aged) were allocated. Spatial learning and memory abilities were tested by Morris water maze. The structure of hippocampal CA1 region was observed by light microscopy. The expression of synaptophysin (SYP) and glial fibrillary acidic protein (GFAP) in hippocampal CA1 region were measured by immunohistochemistry. Results showed that the rat offspring of LPS group needed longer escape latency and path-length in the Morris water maze and presented a significant neuron loss, decreased expression of SYP, increased expression of GFAP in CA1 region in histological studies. All these changes were more significant with the age increasing. These findings support the hypothesis that maternal systemic inflammation may alter the state of astrocytes in rat offspring for a long time, the alteration may affect neurons and synapse development in neural system, increase the neurons' vulnerability to environment especially as the age increasing, at last result in distinct learning and memory impairment.
authors.affiliation: Department of Pharmaceutics, Institute of Materia Medica, College of Pharmacy, Third Military Medical University, Chongqing 400038, PR China.
authors.forename: L Y
authors.initials: LY
authors.lastname: Hao
authors.forename: X Q
authors.initials: XQ
authors.lastname: Hao
authors.forename: S H
authors.initials: SH
authors.lastname: Li
authors.forename: X H
authors.initials: XH
authors.lastname: Li
mesh_terms: D000367:Age Factors; D000818:Animals; D003072:Cognition Disorders / Q000209:etiology / Q000473:pathology / Q000523:psychology*; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D007249:Inflammation / Q000150:complications; D008070:Lipopolysaccharides / Q000494:pharmacology*; D018782:Maze Learning; D008568:Memory; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious; D011297:Prenatal Exposure Delayed Effects / Q000209:etiology / Q000473:pathology / Q000523:psychology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016708:Synaptophysin / Q000096:biosynthesis
chemical_list: D005904:Glial Fibrillary Acidic Protein; D008070:Lipopolysaccharides; D016708:Synaptophysin