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Cerebral Cortex Advance Access originally published online on March 28, 2004
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Cerebral Cortex May 2004; 14:562-574
© Oxford University Press 2004

Article

Localization of the Glutamine Transporter SNAT1 in Rat Cerebral Cortex and Neighboring Structures, With a Note on its Localization in Human Cortex

Marcello Melone1, Fiorinta Quagliano1, Paolo Barbaresi1, Hélène Varoqui2, Jeffrey D. Erickson2 and Fiorenzo Conti1

1 Department of Neuroscience, Section of Human Physiology, Università Politecnica delle Marche, 60020 Ancona, Italy, 2 Neuroscience Center, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA

SNAT1 mediates glutamine (Gln) influx into neurons and is believed to replenish the transmitters pools of glutamate (Glu) and {gamma}-aminobutyric acid (GABA). We investigated its distribution and cellular localization in the cerebral cortex and neighboring regions of rats and humans using light and electron microscopic immunocytochemical methods with specific antibodies. In the first somatic sensory cortex of rats and in areas 9, 10, 21 and 46 of the human cortex, numerous SNAT1-positive (+) cells were present in the cortical parenchyma and in the white matter; >95% of SNAT1+ cells were neurons, but some were astrocytes. Most SNAT1+ cells were pyramidal neurons, but numerous non-pyramidal neurons were also observed: SNAT1/GABA double-labeling studies showed that SNAT1 is expressed in all GABA+ neurons. SNAT1/synaptophysin studies showed that <0.1% of all synaptophysin+ puncta coexpressed SNAT1. SNAT1 immunoreactivity (ir) was also in leptomeninges, ependymal cells and choroid plexus. Electron microscopic studies showed that neuronal SNAT1 ir was almost exclusively observed in perikarya and dendritic profiles. SNAT1 ir was also in distal astrocytic processes, including end feet profiles, and in leptomeninges. These findings suggest that the major function of SNAT1 is not to replenish the transmitter pools of Glu and GABA.


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