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Microglia express GABA B receptors to modulate interleukin release

2004; Elsevier BV; Volume: 25; Issue: 2 Linguagem: Inglês

10.1016/j.mcn.2003.10.023

1095-9327

Susanne Kuhn, Frank van Landeghem, Robert Zacharias, Katrin Färber, Angelika Rappert, Sanja Pavlović, Anja Hoffmann, Christiané Nolte, Helmut Kettenmann,

Tryptophan and brain disorders

gamma-Aminobutyric acid (GABA) can act as a neuroprotective agent besides its well-established role as the main inhibitory neurotransmitter in the CNS. Here we report that microglial cells express GABA(B) receptors indicating that these prominent immunocompetent cells in the brain are a target for GABA. Agonists of GABA(B) receptors triggered the induction of K(+) conductance in microglial cells from acute brain slices and in culture. Both subunits of GABA(B) receptors were identified in cultured microglia by Western blot analysis and immunocytochemistry, and were detected on a subpopulation of microglia in situ by immunohistochemistry. In response to facial nerve axotomy, we observed an increase in GABA(B) receptor expressing microglial cells in the facial nucleus. We activated microglial cells in culture with lipopolysaccharide (LPS) to induce the release of interleukin-6 and interleukin-12p40. This release activity was attenuated by simultaneous activation of the GABA(B) receptors indicating that GABA can modulate the microglial immune response.