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An A to G point mutation at position 112 was created in a BAC harboring exon 1, which corresponds to the SNP position 118 in the human sequence, and changes codon 38 from asparigine to aspartic acid (N38D). A second mutation (T108C) was introduced to abolish a BstXI restriction site without affecting the aspartic acid encoded by the codon. A floxed neomycin cassette was inserted downstream of the targeted exon and was later removed by crossing founder mice with cre transgenic mice. Protein expression in the thalamus of homozygote mice was reduced compared to mice carrying the wild-type allele. (J:150840)