Search Criteria: Research Area is "Neurobiology Research: Receptor Defects: opiod"

JAX® Mice Strains

Stock
Number
Strain Name
 
Strain Description
Standard Supply
007558 B6.129S2-Oprk1tm1Kff/J
Repository- Live
Mice homozygous for this kappa-opioid receptor mutant allele (KOR-) are viable and fertile. KOR-selective ligand binding is absent on brain membranes from homozygous mice. In contrast to mutant mice deficient of delta- or mu-opioid receptors (Stock No. 007557 or 007559), KOR- homozygotes have normal mechanical pain thresholds, but greatly increased sensitivity to chemical visceral pain. KOR- homozygotes also exhibit normal spontaneous stress responses (unlike delta-opioid receptor null mice). Homozygous KOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. These KOR mutant mice may be useful in studying biological activity of opioids, analgesics, spinally mediated thermal nociception and chemical visceral pain thresholds.

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 mut .....
For more information please see the full phenotype on the strain data sheet

007559 B6.129S2-Oprm1tm1Kff/J
Repository- Live
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 usef .....
For more information please see the full phenotype on the strain data sheet
011130 STOCK Arrb2tm1Rjl/J
Repository- Live
Homozygous Arrb2 (arrestin, beta 2) targeted mutation mice show a significantly increased potentiation and prolongation of the analgesic effect of morphine, suggesting that μ opioid receptor desensitization is impaired. They lack expression of the gene as determined by immunoblot of brainstem, periaqueductal gray tissue, spleen, lung, and skin. These mice may be useful in studies of pain and analgesia.
023852 B6.129X1-Arrb2tm1Rjl/J
Under Development - Now Accepting Orders
Homozygous Arrb2 (arrestin, beta 2) targeted mutation mice show a significantly increased potentiation and prolongation of the analgesic effect of morphine, suggesting that μ opioid receptor desensitization is impaired. They lack expression of the gene as determined by immunoblot of brainstem, periaqueductal gray tissue, spleen, lung, and skin. These mice may be useful in studies of pain and analgesia.
026221 B6.Cg-Oprm1tm1.1Jbwa/J
Under Development - Now Accepting Orders
MOR KI mice contain the amino acid mutation T394A in exon 4 of the opioid receptor, mu 1 (Oprm1) gene. These receptors are expressed throughout the neocortex, thalamus, nucleus accumbens, hippocampus, and amygdala, as well as in the peripheral nervous system, and have been associated with pain sensitivity. The MOR also has an important role in dependence to drugs of abuse, such as opioid, nicotine, cocaine, and alcohol via its modulation of the dopamine system. Binding of these drugs increases the release of beta-endorphins, which subsequently increase release of dopamine and stimulates cravings. T394 of the MOR is a crucial residue for initiation of agonist-induced opioid receptor phosphorylation. Homozygotes are viable and fertile. This mutation alters opioid tolerance and vulnerability to opioid abuse and dependence. Mice exhibit attenuated opioid tolerance, enhanced vulnerability to heroin self-administration, enhanced brain dopamine response to heroin, and enhance .....
For more information please see the full phenotype on the strain data sheet
012431 B6.129-Adrbk2tm1Rjl/J
Cryopreserved - Ready for recovery
Adrbk2 (adrenergic receptor kinase, beta 2; also called GRK3) is the major G protein-coupled receptor kinase family member in olfactory neurons, and mice lacking GRK3 exhibit a deficit in desensitization to olfactants. In homozygous mice, airway smooth muscle cells exhibit supersensitivity to muscarinic agents, and brain neurons exhibit altered kappa opioid receptor-dependent tolerance. Expression is eliminated in olfactory neuroepithelium, brain, and airway smooth muscle cells.
007557 B6.129S2-Oprd1tm1Kff/J
Cryopreserved - Ready for recovery
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 ch .....
For more information please see the full phenotype on the strain data sheet

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