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. 2004 Dec 15;24(50):11404–11415. doi: 10.1523/JNEUROSCI.3834-04.2004

Figure 8.

Figure 8.

SSTR2 gene expression in SSTR2 knock-out/lacZ knock-in mice after focal ischemia. SSTR2 gene expression in wild-type mice (sstr2+/+; A, D) and SSTR2 knock-out/lacZ knock-in mice (sstr2-/-; B, E) subjected to 6 hr permanent MCAO was detected by isotopic in situ hybridization with probes for SSTR2 mRNA (A, D) and lacZ mRNA (B, E), respectively. D, E, Comparison of the ipsilateral and contralateral brain hemispheres reveals increased SSTR2 gene expression levels in dorsal and ventral penumbral regions (arrows) both in sstr2+/+ (D) and sstr2-/- (E) mice. A, B, Scatter plots showing quantification of hybridization signal intensities (nanoCuries per gram) performed in the area boxed in D and the corresponding contralateral area. A, In 11 sstr2+/+ mice, median values were significantly larger (p < 0.01) on the ipsilateral side (ipsi; 0.90 nCi/mg) than in the contralateral side (contra; 0.33 nCi/mg). B, A significant ipsilateral versus contralateral increase (p < 0.01) was seen also in 14 sstr2-/- mice (ipsi, 1.39 nCi/mg; contra, 0.91 nCi/mg). C, Scatter plot showing relative SSTR2 gene upregulation in the sstr2+/+ and sstr2-/- mice. The fold upregulation was calculated for each animal dividing ipsilateral by contralateral SSTR2 gene expression levels. Note the stronger upregulation in sstr2+/+ mice (median value, 2.7-fold) than in sstr2-/- mice (median value, 1.5-fold). A-C, Median values are indicated by dashed lines.