Abstract
BackgroundTransient postnatal exposure of rodents to the selective serotonin (5-HT) reuptake inhibitor (SSRI) fluoxetine alters behavior and brain 5-HT neurotransmission during adulthood, and also reduces brain arachidonic (ARA) metabolic consumption and protein level of the ARA metabolizing enzyme, cytochrome P4504A (CYP4A). HypothesisBrain 20-hydroxyeicosatetraenoic acid (20-HETE), converted by CYP4A from ARA, will be reduced in adult mice treated transiently and postnatally with fluoxetine. MethodsMale mice pups were injected i.p. daily with fluoxetine (10mg/kg) or saline during P4–P21. At P90 their brain was high-energy microwaved and analyzed for 20-HETE and six other ARA metabolites by enzyme immunoassay. ResultsPostnatal fluoxetine vs. saline significantly decreased brain concentrations of 20-HETE (−70.3%) and 15-epi-lipoxin A4 (−60%) in adult mice, but did not change other eicosanoid concentrations. ConclusionsBehavioral changes in adult mice treated postnatally with fluoxetine may be related to reduced brain ARA metabolism involving CYP4A and 20-HETE formation.
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