Inflammatory Animal Model for Parkinson's Disease: The Intranigral Injection of LPS Induced the Inflammatory Process along with the Selective Degeneration of Nigrostriatal Dopaminergic Neurons
Figure 1
Effect of LPS on glial cells and dopaminergic neurons. (a) Injection of vehicle within the SN; (b) injection of LPS. OX-6 is a commercial antibody directed against a monomorphic determinant of the rat major histocompatibility complex (MHC) class II antigens, expressed by activated microglia but not for the resting cells. LPS increases OX-6 immunoreactivity around the injection track, filling the area of activated microglia characterized by its round morphology. On the contrary, there is an area lacking GFAP immunoreactivity, a marker of astroglia, around the injection site of LPS. As hallmark of this model, LPS induces the loss of dopaminergic (TH positive) neurons in the SN. Scale bar: 500 μm. (c) Represents the average values of some parameters in the SN (as percentage of controls) after the single injection of 2 μg of LPS: DA/TH/DAT, dopamine content, neurons expressing tyrosine hydroxylase, and dopamine transporter; OX-42/OX-6, density of activated microglial cells; amounts of the proinflammatory cytokines TNF-α and IL-1β, the adhesion molecule ICAM-1, the inducible nitric oxide synthase (iNOS), and the heat shock protein (HSP)-70; the phosphorylated (active) forms of the MAP kinases p38 (associated with promotion of apoptosis) and Akt (cell surviving signal). Alterations on the expression of GFAP and the endothelial barrier antigen (EBA), as area lacking expression (in mm2), are also shown.
