Microglia express GABAB receptors to modulate interleukin release


  • S.A. Kuhn
  • F.K. Van Landeghem
  • R. Zacharias
  • K. Faerber
  • A. Rappert
  • S. Pavlovic
  • A. Hoffmann
  • C. Nolte
  • H. Kettenmann


  • Molecular and Cellular Neuroscience


  • Mol Cell Neurosci 25 (2): 312-322


  • γ-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 GABAB receptors indicating that these prominent immunocompetent cells in the brain are a target for GABA. Agonists of GABAB receptors triggered the induction of K+ conductance in microglial cells from acute brain slices and in culture. Both subunits of GABAB 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 GABAB 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 GABAB receptors indicating that GABA can modulate the microglial immune response.