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- W2012884927 abstract "Fluoxetine is a selective serotonin (5-HT) reuptake inhibitor that, when given chronically, alters different neurotransmitter systems. To assess functional changes occurring in the 5-HT and dopaminergic systems, we investigated the effects of 5-HT(1A) agonist 8-hydroxy-2(di-N-propylamino)tetralin (8-OH-DPAT), of the 5-HT(2A/2C) agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and of the dopamine D(1/2) agonist apomorphine (APO) on behavior and on regional cerebral metabolic rates for glucose (rCMRglc) in rats pretreated for 3weeks with saline or fluoxetine (8mg/kg/day). Behavioral effects were assessed for 8-OH-DPAT by scoring the 5-HT syndrome, for DOI by counting head shakes and for APO with an activity monitor. rCMRglc were measured with quantitative autoradiographic [(14)C]2-deoxyglucose technique in 60 brain regions at 10min after acute administration of 8-OH-DPAT 1mg/kg, at 30min after DOI 5mg/kg or at 10min after APO 1mg/kg. Chronic fluoxetine did not alter the 5-HT syndrome by 8-OH-DPAT, decreased head shakes by DOI and enhanced hyperlocomotion by APO. 8-OH-DPAT produced rCMRglc increases in sensorimotor regions that were unaffected by fluoxetine pretreatment and diffuse metabolic decrements that were attenuated by fluoxetine in limbic and raphe areas (17% and 4% mean decreases, respectively, in saline control and fluoxetine-pretreated rats). DOI produced widespread rCMRglc declines that were intensified by fluoxetine (14% and 20% decreases, in control and fluoxetine rats). APO caused rCMRglc increases in 22 brain regions that were potentiated by fluoxetine in dopaminergic motor areas (10% and 25% increases, in control and fluoxetine rats). In conclusion, fluoxetine enhances 5-HT neurotransmission by blunting responsivity of 5-HT(1A) autoreceptors and increasing that of 5-HT(2A/2C) postsynaptic receptors and enhances dopaminergic D(1/2) receptor neurotransmission." @default.
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- W2012884927 date "2010-06-01" @default.
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- W2012884927 title "Chronic treatment with fluoxetine decreases cerebral metabolic responses to the 5-HT1A agonist 8-hydroxy-2(di-N-propylamino)tetralin and increases those to the 5-HT2A/2C agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane and to the dopaminergic agonist apomorphine" @default.
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- W2012884927 doi "https://doi.org/10.1016/j.brainres.2010.03.090" @default.
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