摘要: Lansbury and Caughey state in their Primer on prion proteins [1xSee all References[1] “Mice lacking the PrP gene, first produced by Charles Weissmann colleagues, are viable, but have altered neuronal function develop neurological abnormalities later life.” This statement is misleading.The PrP-knockout mice our laboratory [2xNormal development behaviour of cell-surface protein. Bueler, H, Fischer, M, Lang, Y, Bluethmann, Lipp, HP, DeArmond, SJ et al. Nature. 1992; 356: 577–582Crossref | PubMed Scopus (1045)See References[2] do not show at any time we never reported such an effect. Moreover, no structural were found independent line generated Manson [3x129/Ola carrying a null mutation that abolishes mRNA production developmentally normal. Manson, JC, Clarke, AR, Hooper, ML, Aitchinson, L, McConnell, I, Hope, J. Mol Neurobiol. 1994; 8: 121–127Crossref (393)See References[3].The phenomenon referred to was observed only Sakaguchi [4xLoss cerebellar Purkinje cells aged homozygous for disrupted gene. Sakaguchi, S, Katamine, Nishida, N, Moriuchi, R, Shigematsu, K, Sugimoto, T 1996; 380: 528–531Crossref (380)See References[4] which coding region also part large intron deleted. It possible attribute phenotype ablation because correction through introduction PrP-expressing cDNA has been carried out. Electrophysiological changes [[5]xRescue neurophysiological seen transgene encoding human Whittington, MA, Sidle, KCL, Gowland, Meads, J, Hill, AF, Pulman, MA Nature Genet. 1995; 9: 197–201Crossref (119)See References, [6]xPrP gene dosage long term potentiation. Clark, Johnston, A, Black, C, Macleod, N. Neurodegeneration. 4: 113–115Crossref PubMedSee References] two different lines PrP-null mice, ours those al., these reflected deficits.