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Microglia express GABA(B) receptors to modulate interleukin release
Susanne A Kuhn1, Frank K H van Landeghem, Robert Zacharias
1Department of Cellular Neuroscience, Max-Delbrück-Center for Molecular Medicine, D-13125 Berlin, Germany.
Molecular and Cellular Neurosciences
|March 17, 2004
Summary
Gamma-aminobutyric acid (GABA) acts on GABA(B) receptors in microglial cells, modulating their immune response. This suggests GABA
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the CNS.
- GABA also exhibits neuroprotective properties.
- Microglia are the resident immune cells of the brain.
Purpose of the Study:
- To investigate the presence and function of GABA(B) receptors in microglial cells.
- To determine if GABA can modulate microglial immune responses.
Main Methods:
- Western blot analysis and immunocytochemistry to detect GABA(B) receptor subunits in cultured microglia.
- Immunohistochemistry to detect GABA(B) receptors in microglia in situ.
- Electrophysiology to measure K+ conductance in microglia.
- Facial nerve axotomy model to study microglial response in vivo.
- Lipopolysaccharide (LPS) stimulation of microglia in culture.
Main Results:
- Microglial cells express both subunits of GABA(B) receptors.
- GABA(B) receptor activation induced K+ conductance in microglia.
- GABA(B) receptor expression increased in microglia after facial nerve axotomy.
- GABA(B) receptor activation attenuated LPS-induced release of IL-6 and IL-12p40 from microglia.
Conclusions:
- Microglia express functional GABA(B) receptors, making them a target for GABA.
- GABA can modulate microglial immune responses, suggesting a role in neuroinflammation.