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Fig. 7 | Molecular Brain

Fig. 7

From: Pharmacological and chemogenetic orexin/hypocretin intervention ameliorates Hipp-dependent memory impairment in the A53T mice model of Parkinson’s disease

Fig. 7

Immunofluorescence (IF) analysis of hippocampal GFAP and IBA1 expression and IBA1 positive cell density in CA1 Hipp region. Representative IF microphotographs of the DAPI, p-α-syn, GFAP, IBA1 and merged image in 5-mo WT aCSF-treated mice (a), WT orexin A-treated mice (b), A53T aCSF-treated mice (e), and A53T orexin A-treated mice (f); Representative IF microphotographs of the DAPI, p-α-syn, GFAP, IBA1 and merged image in 5-mo orx-Cre cDREADD CNO-treated mice (c), orx-Cre qDREADD CNO (d), orx-Cre/A53T cDREADD CNO (g), and orx-Cre/A53T qDREADD CNO mice (h). Representative high-magnification (20x) IF images (b, d) were used for densitometry analysis. Image J was used to quantify the intensity of GFAP and IBA1 staining and density of IBA1 positive cells. Neither orexin A nor orexin neuron specific DREADD intervention had any effect on inflammation (j, k, m, n) and astrogliosis (i, l) (n = 5/group; one-way ANOVA, Tukey’s; *p < 0.05, **p < 0.01, ***p < 0.005)

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