These Oprm1tm1Kff (or MOR-) knock-out mice exhibit a lack of morphine analgesia, reward, and withdrawal. These knock-out mice may be useful in studying the biological activity of opioids, analgesics, and responses to mechanical, chemical and thermal nociception at a supraspinal level.
Brigitte L. Kieffer, McGill University
Mice homozygous for the mu-opioid receptor mutant allele Oprm1tm1Kff (or MOR-) are viable and fertile. MOR-selective ligand binding is absent on brain membranes from homozygous mice. Homozygous mice exhibit a lack of morphine analgesia, reward, and withdrawal. This is accompanied by decreased mechanical, thermal, and chemical pain thresholds. Homozygous mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. In contrast to mutant mice deficient of delta- or kappa-opioid receptors (Stock Nos. 007557 or 007558, respectively), Oprm1tm1Kff homozygotes exhibit hypolocomotive spontaneous stress responses. Indeed, the reduced anxiety and depressive-like behavior observed in Oprm1tm1Kff mutants is in stark contrast to kappa-opioid receptor deficient mice. These knock-out mice may be useful in studying the biological activity of opioids, analgesics, and responses to mechanical, chemical and thermal nociception at a supraspinal level.
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. 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 insert a PGK-neo cassette into exon 2 of the targeted gene. The construct was electroporated into 129S2/SvPas-derived P1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric mice were bred with C57BL/6 mice. These mu-opioid receptor (MOR) 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 to the C57BL/6J genetic background.
|Allele Name||targeted mutation 1, Brigitte L Kieffer|
|Allele Type||Targeted (Null/Knockout)|
|Gene Symbol and Name||Oprm1, opioid receptor, mu 1|
|Strain of Origin||129S2/SvPas|
|Molecular Note||A neomycin selection cassette was inserted into exon 2. Binding assays on brain of homozygous animals confirmed that no functional protein was made from this allele.|
|Mutations Made By|| |
Brigitte Kieffer, McGill University
When maintaining a live colony, heterozygous or homozygous mice may be bred.
When using the MOR- mouse strain in a publication, please cite the originating article(s) and include JAX stock #007559 in your Materials and Methods section.