6533b871fe1ef96bd12d11ce
RESEARCH PRODUCT
Characterization of the transporterB0AT3 (Slc6a17) in the rodent central nervous system.
Robert FredrikssonOlga StephanssonSofie V. HellstenAnna LjungdahlSimons SvirskisJuris RumaksVija KlusaHelgi B. SchiöthSonja WinnergrenSonchita BagchiMaria HägglundVictor C. O. Nilssonsubject
Central Nervous SystemMaleSerotonin reuptake inhibitorVesicular glutamate transporter 1Central nervous systemVesicular Transport ProteinsNerve Tissue ProteinsIn situ hybridizationPharmacology and ToxicologyPharmacologyBiologyPlasma Membrane Neurotransmitter Transport ProteinsRats Sprague-DawleyCellular and Molecular NeuroscienceGlutamatergicMiceDopaminePregnancyMonoaminergicmedicineAnimalsRats WistarCells CulturedNeuronsGeneral NeuroscienceNeurosciencesTransporterFarmakologi och toxikologiEmbryo MammalianAntidepressive AgentsRatsMice Inbred C57BLProtein Transportmedicine.anatomical_structureGene Expression Regulationbiology.proteinFemaleFood DeprivationNeurovetenskapermedicine.drugResearch Articledescription
Abstract Background The vesicular B0AT3 transporter (SLC6A17), one of the members of the SLC6 family, is a transporter for neutral amino acids and is exclusively expressed in brain. Here we provide a comprehensive expression profile of B0AT3 in mouse brain using in situ hybridization and immunohistochemistry. Results We confirmed previous expression data from rat brain and used a novel custom made antibody to obtain detailed co-labelling with several cell type specific markers. B0AT3 was highly expressed in both inhibitory and excitatory neurons. The B0AT3 expression was highly overlapping with those of vesicular glutamate transporter 2 (VGLUT2) and vesicular glutamate transporter 1 (VGLUT1). We also show here that Slc6a17mRNA is up-regulated in animals subjected to short term food deprivation as well as animals treated with the serotonin reuptake inhibitor fluoxetine and the dopamine/noradrenaline reuptake inhibitor bupropion. Conclusions This suggests that the B0AT3 transporter have a role in regulation of monoaminergic as well as glutamatergic synapses.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2013-01-01 | BMC neuroscience |