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RESEARCH PRODUCT
Prenatal low-level exposure to CO alters postnatal development of hippocampal nitric oxide synthase and haem-oxygenase activities in rats.
Luca SteardoLuigia TrabaceAndrea VaccariMauro FàRaffaele CagianoPierluigi SabaAddolorata ColucciaMaria TattoliStefania RuiuVincenzo CuomoGiampaolo Mereusubject
Gene isoformmedicine.medical_specialtyNitric Oxide Synthase Type IHippocampal formationHippocampusCarbon monoxide; haem-oxygenase; hippocampus; nitric oxide synthase; prenatal exposure.HemoglobinsPregnancyInternal medicinemedicineAnimalsPharmacology (medical)Rats WistarPharmacologyDevelopmental profilePregnancyCarbon MonoxidebiologyChemistryLong-term potentiationLow level exposuremedicine.diseaseHaem OxygenaseRatsNitric oxide synthaseIsoenzymesPsychiatry and Mental healthEndocrinologyPrenatal Exposure Delayed EffectsHeme Oxygenase (Decyclizing)biology.proteinFemaleNitric Oxide Synthasedescription
The effects of prenatal CO exposure (150 ppm from days 0 to 20 of pregnancy) on the postnatal development of hippocampal neuronal NO synthase (nNOS) and haem-oxygenase (HO-2) isoform activities in 15-, 30- and 90-d-old rats were investigated. Unlike HO-2, hippocampal nNOS activity increased from postnatal days 15-90 in controls. Prenatal CO produced a long-lasting decrease in either nNOS or HO-2. The results suggest that the altered developmental profile of hippocampal nNOS and HO-2 activities could be involved in cognitive deficits and long-term potentiation dysfunction exhibited by rats prenatally exposed to CO levels resulting in carboxyhaemoglobin (HbCO) levels equivalent to those observed in human cigarette smokers.
year | journal | country | edition | language |
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2001-04-30 | The international journal of neuropsychopharmacology |