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Acta Physiologica 2012; Volume 206, Supplement 691
Scandinavian Physiological Society's Annual Meeting
8/24/2012-8/26/2012
Helsinki, Finland
DIFFERENT GABA-A RECEPTOR SUBUNITS ARE EXPRESSED IN HUMAN, RAT AND MOUSE T LYMPHOCYTES
Abstract number: P02
BHANDAGE1 A, MENDU1 SK, JIN1 Z, BIRNIR1 B
1Box 593, SE 751 24, Div. of Molecular Physiology and Neuroscience, Department of Neuroscience, Biomedical Center, Uppsala University, Uppsala, Sweden
Introduction: g-aminobutyric acid (GABA) is the most abundant inhibitory neurotransmitter in the brain where it acts on synaptic and extrasynaptic GABA-A receptors (GABA-A channels). Recently, different components of the GABA signaling system have also been identified in immune cells which suggest that GABA might have an immunomodulatory role in the immune system. AIM: To examine whether different GABA-A channel subunits are present and functional GABA-A channels are formed in human, mouse and rat CD4+ and CD8+ T cells and Jurkat cells.
Methods:
RT-qPCR, Western blot, immunocytochemistry and patch-clamp techniques were used.
Results:
There were 5, 8 and 13 different GABA-A subunit mRNAs identified in human, mouse and rat CD4+ and CD8+ T cells, respectively. Importantly, the g2 subunit that imposes benzodiazepine sensitivity on the GABA-A channel was only detected in the mouse T cells. The presence of GABA-A channel subunits was further confirmed at the protein level. Immunolabeling of GABA-A channel subunits (e.g. a1) was observed in both in the cytoplasm and in the plasma membrane. GABA-evoked currents were recorded in rat T cells and Jurkat cells.
Conclusion:
In T cells from both humans and rodents, GABA-A channels are expressed and functional but the GABA-A channel subtypes varies between the species. This is important to bear in mind when selecting the appropriate animal models to study the physiological and pharmacological roles GABA-A channels have in the CD4+ and CD8+ T cells.
To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 691 :P02