These delta-opioid receptor deficient mice exhibit increased anxiety and depressive-like behavior. They also have increased ethanol self-administration and increased inflammatory pain.
Brigitte L. Kieffer, McGill University
Mice homozygous for this delta-opioid receptor mutant allele (DOR-) are viable and fertile. DOR-selective ligand binding is absent in vitro on brain membranes from homozygous mice. Unlike mutant mice deficient in kappa- or mu-opioid receptors (Stock No. 007558 or 007559, respectively), homozygous DOR- mutants exhibit increased anxiety and depressive-like behavior but no alteration of spontaneous pain perception. Homozygous DOR- mice also have increased ethanol self-administration and increased inflammatory pain. These DOR mutant mice may be useful in studying the biological activity of opioids andanalgesics, mechanical nociception, inflammatory pain, and emotional disorders.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. These mutant mice were originally published on a mixed genetic background, and the donating investigator reports that increased anxiety may not be observable on this congenic background. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
A targeting vector was designed to replace the entire first exon (amino terminal region and ATG translation initiation codon) of the targeted gene with a PGK-neo cassette. The donating investigator reports that the construct was electroporated into 129S2/SvPac-derived embryonic stem (ES) cells, and correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric males were bred with C57BL/6 females. These delta-opioid receptor (DOR) mutant mice were backcrossed to C57BL/6J inbred mice for at least 12 generations prior to arrival at The Jackson Laboratory. The Y chromosome may not have been fixed for the C57BL/6J genetic background.
|Allele Name||targeted mutation 1, Brigitte L Kieffer|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||DOR-; Oprd1-|
|Gene Symbol and Name||Oprd1, opioid receptor, delta 1|
|Strain of Origin||129/Sv|
|Molecular Note||Exon 1, which encodes the translational start codon, was replaced by a neomycin selection cassette inserted by homologous recombination. A radiolabeled binding assay demonstrated complete functional ablation in homozygous mutant mice.|
|Mutations Made By|| |
Brigitte Kieffer, McGill University
When maintaining a live colony, heterozygous or homozygous mice may be bred.
When using the Oprd1 KO mouse strain in a publication, please cite the originating article(s) and include JAX stock #007557 in your Materials and Methods section.