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Figure 1 | Journal of Neuroinflammation

Figure 1

From: Microglial MAC1 receptor and PI3K are essential in mediating β-amyloid peptide-induced microglial activation and subsequent neurotoxicity

Figure 1

Absence of MAC1 attenuates Aβ-induced dopaminergic and GABAergic neurotoxicity in neuron-glia cultures. Mice (MAC1+/+ and MAC1-/-) mesencephalic neuron-glia cultures in 24-well plates were treated with vehicle medium (control group) or 0.5 μM, 1.0 μM and 2.0 μM Aβ for 7 days. (A) Aβ-induced dopaminergic neurotoxicity was quantified by [3H] dopamine uptake assay. (B) Numbers of TH-positive cells remaining in the neuron-glia cultures after vehicle or Aβ treatment. (D) Representative light microscopic images are shown for TH-positive neurons treated with vehicle or Aβ. Scale bar: 100 μm. (C) Mice (MAC1+/+ and MAC1-/-) cortical neuron-glia cultures in 24-well plates were treated with vehicle or 1.0 μM, 2.0 μM and 4.0 μM Aβ for 7 days. Aβ-induced GABAergic neurotoxicity was quantified by [3H] GABA uptake assay. (E) Mice (MAC1+/+ and MAC1-/-) mesencephalic microglia-depleted cultures in 24-well plates were treated with vehicle medium (control group) or 1.0 μM, 2.0 μM and 4.0 μM Aβ for 7 days. Aβ-induced dopaminergic neurotoxicity was quantified by [3H] dopamine uptake assay. Results are from four independent experiments. #: p < 0.05 compared with corresponding vehicle-treated controls. *: p < 0.05 compared with MAC1+/+ cultures after same treatments.

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