논문 초록

Molecular markers for GABAergic and non GABAergic astrocyte
In our recent study, we reported that tonic inhibition in the cerebellum is due to GABA being released from GFAP positive glial cells by permeation through the Bestrophin 1 (Best1) anion channel. Our immunohistochemistry data using anti-GABA antibody in GFAP-GFP mouse brain section revealed that GFP positive glial cells show strong GABA immunoreactivity in cerebellum but was absent in hippocampus. Based on these findings, we next asked how glial GABA is synthesized or where glial GABA comes from. There are several potential pathways for GABA production in glial cells. First, GABA can simply come from GABA uptake into glial cells by GABA transporters. Second, glutamate decarboxylase (GAD) which synthesizes GABA from glutamate can produce GABA in glial cells, just like neurons. Third, the presence or absence of GABA-transaminase (GABA-T) which catalyzes the conversion of GABA and 2-oxoglutarate into succinic semi-aldehyde and glutamate can determine the amount of GABA in glial cells. Finally, GABA might be derived from the mono-acetylation of putrescine. We have tested each possible pathway using electrophysiology, immunohistochemistry, micro-dialysis and HPLC by comparing hippocampal and cerebellar glial cells.
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