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Late N-acetylcysteine treatment prevents the deficits induced in the offspring of dams exposed to an immune stress during gestation
Hippocampus, 2008-01, Vol.18 (6), p.602-609
Lanté, Fabien
Meunier, Johann
Guiramand, Janique
De Jesus Ferreira, Marie-Céleste
Cambonie, Gilles
Aimar, Rose
Cohen-Solal, Catherine
Maurice, Tangui
Vignes, Michel
Barbanel, Gérard
2008
Details
Autor(en) / Beteiligte
Lanté, Fabien
Meunier, Johann
Guiramand, Janique
De Jesus Ferreira, Marie-Céleste
Cambonie, Gilles
Aimar, Rose
Cohen-Solal, Catherine
Maurice, Tangui
Vignes, Michel
Barbanel, Gérard
Titel
Late N-acetylcysteine treatment prevents the deficits induced in the offspring of dams exposed to an immune stress during gestation
Ist Teil von
Hippocampus, 2008-01, Vol.18 (6), p.602-609
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2008
Link zum Volltext
Quelle
Wiley Online Library - AutoHoldings Journals
Beschreibungen/Notizen
Prenatal infection is a major stressful experience leading to enhanced susceptibility for mental illnesses in humans. We recently reported in rats, that oxidative stress and glutathione (GSH) shortage occurred in fetal male brain after lipopolysaccharide (LPS) to the dams and that these responses might be involved in the neurodevelopmental deficits observed in adolescent offspring. Furthermore, pretreatment with N‐acetylcysteine (NAC) before LPS avoided both delayed synaptic plasticity and mnesic performance deficits. Since NAC is one of the few medications permitted in pregnant women, this study evaluated the ability of NAC to serve as a protective therapy even after the LPS challenge. Pregnant rats received a single ip injection of E. coli LPS, two days before delivery, and were given NAC in their tap water after the LPS. GSH was evaluated at the time of its expected drop in the hippocampus of male fetuses, whereas long‐term potentiation (LTP) in the CA1 area of the hippocampus and spatial memory in the water‐maze were recorded in 28‐day‐old male offspring. Post‐treatment with NAC, four hours after the LPS challenge fully prevented the drop in the GSH hippocampal content. LTP, as well as spatial learning were completely protected. NAC administration at delivery also partially restored the LTP whereas post‐treatment two days later was inefficient. Another set of dams were supplemented with α‐tocopherol prior to LPS exposure, enhancing the α‐tocopherol levels in fetal hippocampus. This treatment did not prevent the LPS‐induced synaptic plasticity impairment. These results point to fetal hippocampal GSH as a major target of the detrimental effects of in utero LPS challenge. The therapeutic window of NAC extends up to birth, suggesting that this drug might be clinically useful even after an immuno‐inflammatory episode. © 2008 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 1050-9631
eISSN: 1098-1063
DOI: 10.1002/hipo.20421
Titel-ID: cdi_hal_primary_oai_HAL_hal_00397553v1
Format
–
Schlagworte
Acetylcysteine
,
Acetylcysteine - administration & dosage
,
Acetylcysteine - pharmacology
,
Acetylcysteine - therapeutic use
,
alpha-Tocopherol
,
alpha-Tocopherol - administration & dosage
,
alpha-Tocopherol - analysis
,
alpha-Tocopherol - therapeutic use
,
Animals
,
Antioxidants
,
Antioxidants - administration & dosage
,
Antioxidants - pharmacology
,
Antioxidants - therapeutic use
,
Drug Administration Schedule
,
Drug Evaluation, Preclinical
,
Endotoxemia
,
Endotoxemia - drug therapy
,
Endotoxemia - immunology
,
Endotoxemia - physiopathology
,
Female
,
Glutathione
,
Glutathione - analysis
,
Glutathione - deficiency
,
GSH
,
Hippocampus
,
Hippocampus - chemistry
,
Hippocampus - embryology
,
Hippocampus - pathology
,
Life Sciences
,
Lipopolysaccharides
,
Lipopolysaccharides - toxicity
,
Long-Term Potentiation
,
Long-Term Potentiation - drug effects
,
Long-Term Potentiation - physiology
,
LPS
,
Male
,
Maternal Exposure
,
Maze Learning
,
Maze Learning - drug effects
,
Maze Learning - physiology
,
Memory Disorders
,
Memory Disorders - etiology
,
Memory Disorders - physiopathology
,
Memory Disorders - prevention & control
,
Neurons and Cognition
,
Neuroprotective Agents
,
Neuroprotective Agents - administration & dosage
,
Neuroprotective Agents - pharmacology
,
Neuroprotective Agents - therapeutic use
,
oxidative stress
,
Pregnancy
,
Pregnancy Complications
,
Pregnancy Complications - drug therapy
,
Pregnancy Complications - immunology
,
Prenatal Exposure Delayed Effects
,
Prenatal Exposure Delayed Effects - physiopathology
,
Prenatal Exposure Delayed Effects - prevention & control
,
Rats
,
Rats, Sprague-Dawley
,
synaptic plasticity
,
water maze
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