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It is noteworthy that these anti-inflammatory effects exerted by dopaminergic signaling in astrocytes are mediated by D1R and D2R, while D3R mediates the pro-inflammatory effects ( D1R D1R signaling participates in the negative regulation of the activation of NLRP3 inflammasome, which can be assembled upon stimulation with accumulated endogenous metabolites such as fibrillar amyloid and 25-hydroxycholesterol (113), the subsequent secretion of caspase-1 and IL-1 contributes to the destruction of dopaminergic neurons (114)

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