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Figure 3 | Molecular Brain

Figure 3

From: Impaired synaptic clustering of postsynaptic density proteins and altered signal transmission in hippocampal neurons, and disrupted learning behavior in PDZ1 and PDZ2 ligand binding-deficient PSD-95 knockin mice

Figure 3

Altered expression of SAP102 and PSD-93 in the hippocampus of KI mice. A, Immunoblot analyses of hippocampal homogenates from WT and KI mice at the respective developmental ages for the indicated proteins. The following amounts of homogenate proteins were analyzed per lane: PSD-93 and SAP102, WT and KI: 5 μg; GluA1 and GluA2/3, WT and KI: 10 μg; and PSD-95, WT: 5 μg, KI: 20 μg. The arrowhead indicates the degraded bands of PSD-93. B, Quantitation of PSD proteins in the hippocampal homogenates based on the results shown in A, normalized to the wild-type levels at P30 (set as 100%). The histograms show the mean ± SEM (open bars, WT; filled bars, KI). Three sets of hippocampal homogenates at various ages (P4–P65) were examined. The means and SEM of WT and KI data were compared using Student’s t-test. *P < 0.05, **P < 0.005, ***P < 0.001. In the KI PSD homogenates, extensively low levels of mutant PSD-95, significantly decreased levels of PSD-93, and increased levels of SAP102 were observed during development compared to the WT mice, while the levels of GluA1 and GluA2/3 were not significantly different from those of the WT mice. C, Northern blot analyses of PSD-95 and SAP102 mRNA. Ten micrograms of total RNA prepared from WT and KI mice hippocampi were analyzed in a formaldehyde-containing 1% agarose gel. The numbers on the left side indicate the sizes of the digoxigenin-labeled RNA molecular weight markers. Arrowheads indicate the major band for each mRNA.

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