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. Author manuscript; available in PMC: 2009 Jul 1.
Published in final edited form as: Nat Neurosci. 2008 Dec 21;12(1):60–69. doi: 10.1038/nn.2238

Figure 3.

Figure 3

The cookie finding phenotype is manifest in PrP knockouts on other genetic backgrounds. (a) Trial 1 of the cookie finding test for B6 (filled) and Nagasaki PrP−/− (open). (b) Trial 2 for mice shown in a. Note the reduced timescale of 5 min. (c) Schematic diagram of genetic background of the B6 wild types and congenic Ng PrP−/−. Black represents alleles of B6 origin, cyan alleles of 129 origin; red cross represents the knockout allele. (d) Individual progression from Trial 1 to Trial 2 of each B6 mouse. (e) Individual progression from Trial 1 to Trial 2 of each Ng PrP−/− mouse. (f) Average degree of improvement for B6 (filled) and Ng PrP−/− (open); error bars ±SEM. (g) Trial 1 of the cookie finding test for Edinburgh PrP+/+ (filled) and Edinburgh PrP−/− (open). (h) Trial 2 for mice shown in g. (i) Schematic diagram of genetic background of the Ed PrP−/− and isogenic WT littermates (129/Ola background). Cyan represents alleles of 129/Ola origin; red cross represents knockout allele. (j) Individual progression from Trial 1 to Trial 2 of each 129/Ola WT mouse. (k) Individual progression from Trial 1 to Trial 2 of each Ed PrP−/− mouse. (l) Average degrees of improvement for Ed PrP−/− (open) and PrP+/+ littermates (filled) were not significantly different due to the low n; error bars ±SEM.

In (a), (b), (e), (f) black lines represent median values; * p<0.05; *** p<0.001, two-tailed Mann Whitney test. In (f): * P<0.05, one-tailed unpaired t test.