Key result
Cerebral ischemia induces microglial D2 receptor expression, while pramipexole enhances microglial nitrite secretion.
Dopamine is the predominant catecholamine in the brain and functions as a neurotransmitter. Dopamine is also a potent immune modulator. In this study, we have characterized the expression of dopamine receptors on murine microglia. We found that cultured primary microglia express dopamine D1, D2, D3, D4, and D5 receptors. We specifically focused on the D2 receptor (D2R), a major target of antipsychotic drugs. Whereas D2Rs were strongly expressed on striatal neurons in vivo, we did not detect any D2R expression on resident microglia in the healthy brains of wild-type mice or transgenic mice expressing the green fluorescent protein (GFP) under the control of the Drd2 promoter. However, cerebral ischemia induced the expression of D2R on Iba1-immunoreactive inflammatory cells in the infarct core and penumbra. Notably, D2R expression was confined to CD45(hi) cells, and GFP BM chimeras revealed that D2R was expressed on activated resident microglia as well as on peripherally derived macrophages in the ischemic brain. Importantly, the D2/3R agonist, pramipexole, enhanced the secretion of nitrite by cultured microglia in response to proinflammatory stimuli. Thus, dopamine may serve as a modulator of microglia function during neuroinflammation.
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Huck et al. (2015) studied Cerebral ischemia (stroke). Cerebral ischemia and pramipexole (D2/3R agonist) vs. Healthy murine brains / unstimulated microglia was evaluated on Expression of dopamine D2 receptors (D2R) on microglia/macrophages and nitrite secretion. Cerebral ischemia induced de novo dopamine D2 receptor expression on activated microglia and macrophages in mice, while pramipexole enhanced microglial nitrite secretion in vitro.
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