Fig 2: GnRH neurons are immunoreactive for GIRK2 (Kir3.2). A, Single confocal plans showing GnRH neurons (red), colabeled with GIRK2 (green; scale bar, 10 µm) in 11-d-old explants (N = 3). Representative pictures showing all GnRH neurons examined were colabeled with the GIRK2 antibody. B, Single confocal plans showing GnRH neurons (red), with background (green) when GIRK2 antibody was omitted and used to set the camera at the level of nonspecific staining; the experiment was run simultaneously with the one shown in the second row in A.

Fig 3: Effect of genotype and spatial memory training on hippocampal levels of GIRK channel subunits and modulator. Protein levels of GIRK channel subunits (1–4) and modulator (RGS7) in the hippocampus of naïve and memory-trained non transgenic (WT) and APPSw,Ind J9 mice at 6 months of age. (A) GIRK1, (B) GIRK2, (C) GIRK3, (D) GIRK4 and (E) RGS7. Data is expressed as percentage relative to untrained naïve WT mice (100%). ** p < 0.01 vs. naïve WT. ßAct, ß actin.

Fig 4: Immunohistological analysis of hVM tissue at 20 weeks post-graft. Immunohistochemistry of TH + ve neurons (brown) and HuNu (blue) in the hVM graft (top panel). From left to right, images depict representative tissue from a Control rat (A), Lesion rat (B) and a large hVM graft (C). The central panel depicts A9 TH + ve neurons (green) co-labelled with Girk2 (red, D); A10 TH + ve neurons (green) co-labelled with Calbindin (red, E); × 10 magnification of hVM cells with TH + ve neurons stained in brown and HuNu + ve cells in blue (F). The bottom panel depicts the number of TH + ve cells per individual graft (G) and as a group mean (H), as well as the proportion of girk2 + ve (I) and calbindin + ve (J) cells out of the total number of TH + ve neurons. Scale bar = 1000 µm. Error bars = ± standard error of mean. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Fig 5: R2-Pep normalize OGD-mediated dysregulation of Kir3.2 channels. Cultures were stressed for 1 h with OGD and immediately treated with R2-Pep, Ctrl-Pep or remained untreated. After 16 h neurons were immunostained for Kir3.2 channel expression. Top: representative images (scale bar: 5 µm). Bottom: quantification of fluorescence intensities. The fluorescence intensity of the untreated neurons served as control. The data represent the mean ± S.E.M. of 37–38 neurons from two independent preparations. ns: p > 0.05; ****, p < 0.0001; two-way ANOVA with Tukey’s multiple comparisons test.