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Acta Physiologica 2008; Volume 193, Supplement 664
Scandinavian Physiological Society’s Annual Meeting 2008
8/15/2008-8/17/2008
Oulu, Finland
EXTRASYNAPTIC-LIKE GABA CHANNELS EXPRESSED IN LYMPHOCYTES
Abstract number: P64
KUMAR MENDU1 S, AKESSON1 L, JIN1 Z, CALCAGNILE1 O, CILIO1 CM, LERNMARK1 Å, BIRNIR1 B
1Lund University, Clinical Research Center, Entry-72, Plan-91-11, Malm 20502, Sweden
Background and aims:
GABA is the predominant inhibitory neurotransmitter in the mammalian central nervous system (CNS) where it binds to GABA-A receptors (GABA channels) and opens their chloride channel. Outside the nervous system, pancreatic alpha cells and lymphocytes may express GABA channels. The GABA concentration in plasma in healthy individuals is around 100 nM. We have shown that extrasynaptic GABA channels are activated by submicromolar GABA concentrations. In this study we examined if CD4+ and CD8+ lymphocytes isolated from mesenteric lymph nodes (MLN) from BB (BioBreeding) rats express GABA channel subunits.
Material and methods:
Lymph nodes were isolated from congenic BBlyp/lyp rats that develop T1D spontaneously and from wildtype BB+/+ rats. Lymphocytes were isolated and CD4+ and CD8+ cells identified and purified. Total RNA was extracted from the cells and brain samples used as a positive control. RNA was reverse transcribed and used in quantitative RT- PCR reactions using GABA-A subunit specific primers.
Results:
Cells isolated from MLN BBlyp/lyp and BB+/+ rats, showed similar pattern of subunit expression with some variation between CD4+ and CD8+ cells. The most prominent expression was observed for alpha1, alpha6, beta3 and delta subunits. Notably, the gamma2 subunit thought to be present in all synaptic receptors was absent. At onset of diabetes, the relative expression of the alpha4 subunit was increased in CD4+ and CD8+ cells whereas the alpha6 expression was decreased.
Conclusions:
The results are consistent with expression of high-affinity, extrasynaptic-like GABA channels in CD4+ and CD8+ lymphocytes. Supported by: Novo Nordisk Foundation, Crawford Foundation, Swedish Research Council
To cite this abstract, please use the following information:
Acta Physiologica 2008; Volume 193, Supplement 664 :P64