Search Criteria: Research Area is "Sensorineural Research: Nociception"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 003770 | B6.129X1-Trpv1tm1Jul/J | Level 4 |
| Mice that are homozygous targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected in dorsal root ganglia. Cultured dorsal root ganglia neurons and skin preparations display no, or markedly attenuated, response to vanilloid compounds, acidified environments or heat (43 degrees C). In intact wild type mice, a subcutaneous injection of vanilloid compounds into the hind paw elicits a pain response with subsequent swelling. No pain response is observed in homozygotes and swelling is noticeably reduced. Also absent is the profound reduction in body temperature following a subcutaneous injection of capsaicin. Homozygotes appear to display robust deficits in thermally evoked pain-related behavior and do not display an aversion to ingesting capsaicin-supplemented drinking water. | ||
| 004104 | FVB.Cg-Mmp9tm1Tvu/J | Level 4 |
| Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of 3-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (6 to 8 times larger vs. wildtype) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by 8 weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses. | ||
| 013127 | B6.129-Accn3tm1Wsh/J | Repository- Live |
| Homozygous Accn3 (amiloride-sensitive cation channel 3) targeted mutation mice display alterations in normal and pain-associated cutaneous mechanosensitivity and inflammatory pain sensation, visual loss associated with night blindness, and age-induced hearing loss. Mice show increased sensitivity of mechanoreceptors detecting light touch. Sensitivity of mechanoreceptors responding to noxious pinch is decreased as is the response of acid- and noxious heat-sensitive nociceptors. No mRNA is detectable by RT-PCR in the dorsal root ganglion. Protein is not found in trigeminal and dorsal root ganglion. This strain may be useful in further elucidating the role of this gene in mechanosensation. | ||
| 010773 | B6.129-Trpv3tm1Apat/J | Repository- Live |
| Homozygous (TRPV3-/-) mice are viable and fertile, with deletion of Trpv3 (transient receptor potential cation channel, subfamily V, member 3) exons resulting in low levels of truncated TRPV3 transcript that does not encode the putative pore region or adjacent transmembrane domains five and six (essential domains of the ion channel). Homozygous mice lack functional TRPV3 with no abnormal affects on TRPV1/TRPV4 expression or overall dorsal root ganglia or skin anatomy. TRPV3-/- mice have strong deficits in responses to innocuous and noxious heat stimuli, but not in other sensory modalities, and retain a residual sensitivity to warm temperatures. Compared to wildtype mice, TRPV3-deficient mice are resistant to the anxiolytic-like and antidepressive-like behavioral effects (and concomitant changes in c-Fos activation in the brain) following treatment of the TRPV3 agonist, incensole acetate. Unlike wildtype keratinocytes, TRPV3-deficient keratinocytes are not a ..... For more information please see the full phenotype on the strain data sheet | ||
| 002928 | B6.129P2-Cd40tm1Kik/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice exhibit impaired immunoglobulin class switching and germinal center formation. | ||
| 009132 | B6.129P2-P2ry2tm1Bhk/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of kidney tissue. Intracellular calcium ion levels in lung fibroblasts isolated from homozygotes fail to respond to nucleotide (UTP, ATP, ADP, UDP) challenge. Isolated airway epithelial cells have a loss of or diminished intracellular calcium response to nucleotide challenge. Unlike wild-type macrophages, macrophages derived from these animals fail to respond to extracellular stimulation with UTP. ATP- and adenosine 50[g-thio] triphosphate (ATPgS)-evoked aortic endothelium-dependent relaxation is reduced. Luminal nucleotide stimulated distal colonic ion transport is reduced. Homozygotes are more susceptible to lung infections of Pseudomonas aeruginosa, exhibit impaired neutrophil chemotaxis (loss in gradient sensing and migration distance), and loss of sensitivity to ..... For more information please see the full phenotype on the strain data sheet | ||
| 008198 | B6.129P2-Trpm8tm1Jul/J | Repository- Live |
| Mice homozygous for this TRPM8 targeted mutation are viable and fertile, with no differences in core body temperature compared to wildtype. Functional TRPM8 transcripts are absent in trigeminal ganglia from homozygous mutants however,a truncated, non-functional transcript is generated. Immunostaining of trigeminal ganglia, corneal afferents, and spinal cord dorsal horn reveals loss of TRPM8 expression in homozygous mutants. TRPM8-deficient mice exhibit behavioral deficits in their ability to discriminate between cold and warm surfaces, or to respond to evaporative cooling. Homozygous mice are not completely cold insensitive as they avoid contact with surfaces below 10 C (albeit with reduced efficiency). Cultured sensory neurons and intact sensory nerve fibers from TRPM8-deficient mice exhibit profoundly diminished responses to cold. These TRMP8 (transient receptor potential cation channel, subfamily M, member 8 (also called TRP melastatin 8 or cold and menthol receptor 1 (CMR1))) muta ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 ..... | ||
| 007559 | B6.129S2-Oprm1tm1Kff/J | Repository- Live |
| Mice homozygous for this mu-opioid receptor mutant allele (MOR-) are viable and fertile. MOR-selective ligand binding is absent on brain membranes from homozygous mice. Homozygous MOR- mice exhibit a lack of morphine analgesia, reward, and withdrawal. This is accompanied by decreased mechanical, thermal, and chemical pain thresholds. Homozygous MOR- 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 No. 007557 or 007558, respectively), MOR- homozygotes exhibit hypolocomotive spontaneous stress responses. Indeed, the reduced anxiety and depressive-like behavior observed in MOR- mutants is in stark contrast to kappa-opioid receptor deficient mice. These MOR mutant 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 ..... | ||
| 002266 | B6.129S4-Bdnftm1Jae/J | Repository- Live |
| Mice heterozygous for the Bdnftm1Jae mutation show about half normal levels of Bdnf mRNA, but appear normal. Mice homozygous for the Bdnftm1Jae mutation are smaller than normal siblings and most die within the second postnatal week. They have defective coordination of movements and balance. They also exhibit head bobbing and spinning during periods of hyperactivity. There are rare survivors to adulthood. There is excessive degeneration in all sensory ganglia examined, including the vestibular ganglion. Motor neurons are not affected. BDNF can prevent death of central motor neurons and other neurons in vitro, but does not affect these in vivo. | ||
| 002213 | B6.129S4-Ngfrtm1Jae/J | Repository- Live |
| Mice homozygous for the Ngfrtm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by four months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a two- to three-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day three, respectively. These ages coincide with the peak of naturally occurring cell death. p75-deficient ..... For more information please see the full phenotype on the strain data sheet | ||
| 007084 | B6.FVB(Cg)-Mmp9tm1Tvu/J | Repository- Live |
| Mice that are homozygous null for the Mmp9 gene are viable and fertile. No Mmp9 activity is detected in spleen cell lysates. Long bones (tibia, femur) are 10% shorter in homozygous null mice. Histological examination of three-week-old mice reveals a dramatically lengthened zone of hypertrophic cartilage (six to eight times larger vs. wild-type) due to delayed apoptosis, vascularization, and ossification. Subsequent remodeling resolves the condition, resulting in normal appearing bones by eight weeks of age. Null mice show altered responses to repair of injury in skin, cornea, central nervous system and bone marrow reconstitution, and altered inflammatory responses.
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. It should be noted that the phenotype could vary from that originally described. We will modify the strain de ..... | ||
| 013041 | B6;129S6-Ppp1r14ctm1Uhl/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that the expected number of homozygotes are produced in heterozygous crosses. No gene product (mRNA) is detected by RT-PCR analysis of brain tissue from homozygotes. SNP analysis revealed that the Oprm1 allele variant, which is located close to the targeted gene, is from C57BL/6. Homozygotes exhibit increased phosphatase 1 activity in the thalamus. Homozygotes develop faster morphine tolerance in a hot plate assay ("supraspinal" nociceptive response assessment) and a rightward shift in dose response curve for morphine reward in conditioned place preference when compared to wildtype controls. | ||
| 003810 | STOCK Adrb1tm1Bkk Adrb2tm1Bkk/J | Repository- Live |
| Mice that are homozygous null for the Adrb1 and Adrb2 genes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Stimulation of beta adrenergic receptor function in these mice by agonists or exercise reveals significant impairments in chronotropic range, vascular reactivity and metabolic rate. A severely attenuated chronotropic and hypotensive response is observed after administration of the non-selective beta adrenergic receptor agonist isoproterenol. An abnormal response to epinephrine is also seen, with bradycardia and a monophasic hypertensive blood pressure change being observed rather than the tachycardia and biphasic hypertensive/ hypotensive response seen in wildtype mice. When exercised, heart rates in null mice are lower than that of wild type mice. No difference is noted in the resting heart rate. | ||
| 014581 | STOCK Trpm8tm1Apat/J | Repository- Live |
| These mutant mice express farnesylated enhanced GFP gene (EGFPf) from the endogenous Trpm8 locus. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No wildtype gene product (mRNA) is detected although low levels of a truncated mRNA splice variant is sometimes detected by RT-PCR analysis of total RNA derived from dorsal root ganglia (DRG) isolated from homozygotes. No Trpm8 locus mRNA is detected by in situ hybridization of DRG isolated from homozygotes. In thermotaxis assays performed in a cage equipped with surface temperature gradients, homozygous mice spend less time in the warmer area compared to wildtype controls. Homozygotes display diminished responses to application of acetone and injection of icilin. Noxious cold sensation of colder temperatures (sub zero) is normal. Mutant mice do not display cold-induced analgesia in response to pain. EGFPf-positive n ..... For more information please see the full phenotype on the strain data sheet | ||
| 002777 | B6.129S2-Adra2atm1Lel/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this mutation are viable and fertile. They exhibit loss of physiological functions evoked by alpha2-adrenergic receptor agonists and display increased susceptibility to kindling-induced seizures. | ||
| 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 ..... | ||
| 004272 | B6.129S4-Pdyntm1Ute/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No targeted gene product (mRNA or protein) was detected by immunoassay or RT/PCR. Pain withdrawal threshold response of mutant mice is similar to that of wildtype mice. Mutant mice exhibit mild hyperalgesia. This mutant mouse strain represents a model that may be useful in studies of the role of dynorphin in pain, substance abuse and epilepsy. | ||
| 004189 | B6.129S4-Prkcetm1Msg/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the Prkcetm1Msg targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous females produce small litters (0-2 pups). Protein kinase C, epsilon protein was not immunodetectable in dorsal root ganglia or in the central nervous system of mutant mice. Homozygous mutant mice exhibit reduced anxiety, reduced alcohol consumption and reduced responses to nociceptive stimuli. The mice are also supersensitive to acute behavioral effects of allosteric Gamma aminobutyrate (GABA) type A receptor activating drugs. This strain represents a model that may be useful in studies of pharmacological agents for the treatment of alcoholism, anxiety and pain. | ||
| 005251 | B6.129X1-Htr3atm1Jul/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of the dorsal root ganglia. Quantitative autoradiography ligand binding assays of solitary tract nucleus, area postrema and trigenimal nucleus caudalis and electrophysiological tests of isolated nociceptor neurons do not detect functional receptor activity. Mutant mice have an impaired response to persistent pain caused by inflammatory tissue injury. This mutant mouse strain may be useful in studies of nociceptive processing, pain response behavior, and peripheral neurogenic inflammation. | ||
| 006337 | B6.Cg-Lgals1tm1Rob/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. No gene product (mRNA or protein) is detected by in situ hybridization of dorsal root ganglia and facial motorneuron nucleus and Western blot analysis of adult muscle tissue. Neonate mice homozygous for the mutation have abnormal axon targeting to the caudal region of the olfactory bulb. Mutant mice have fewer neural progenitor cells in the subventricular zone of the forebrain, although the number of apoptotic cells are not affected. Homozygotes exhibit hypoalgesia with a diminished nocifensive withdraw response to thermal testing. Immunohistological analysis of dorsal root ganglia from homozygotes reveals abnormal proportions of axon subpopulations and a larger number of myelinated axons. Mutant mice have a longer recovery of motorneuron function after experimental nerve injury. This mutant mouse strain represents a model that may be useful in stu ..... For more information please see the full phenotype on the strain data sheet | ||
| 003951 | B6.P2-P2rx3tm1Ckn/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the P2rx3 gene are viable, fertile, normal in size and do not display any gross physical abnormalities. A significantly decreased nociceptive response (hindpaw lifting, licking, biting) is observed in response to injection of ATP, and to a lesser extent formalin. Responses to noxious thermal and mechanical stimuli are similar to that seen in wild-type mice. Aged mice may develop cutaneous hypersensitivity. Mice also exhibit urinary bladder hyporeflexia, characterized by decreased micturition (urination) frequencies and increased bladder capacities. Whole-cell patch-clamp analysis indicates that homozygote null mice lose the rapidly desensitizing ATP-induced currents in dorsal root ganglion. This strain is suitable for use in studies examining afferent sensory pathways. | ||
| 002466 | B6;129P2-Prkcctm1Stl/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Prkcctm1Stl targeted mutation are viable and develop normally. Homozygous mice show diminished long-term potentiation (LTP) in the hippocampus, but two other types of synaptic plasticities are normal, namely long-term depression and paired-pulse facilitation. Despite this diminished LTP capacity homozygotes can learn to do hippocampus-dependant tasks, such as the Morris water maze and context-dependent fear conditioning, with only slight deficits. | ||
| 010535 | B6;129S4-Gabrr1tm1Llu/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes exhibit an increased sensitivity to mechanical pain and a decreased inhibition of stimulation-evoked spinal cord response following GABA application. This mutant mouse strain may be useful in studies of GABA-mediated pain sensory pathways. | ||
| 005408 | C;129P2-Npy1rtm1Pern/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile and do not display any gross behavioral abnormalities. At age 3 to 5 months female mutant mice exhibit increased body weight. Northern blot analysis detects mRNA encoding beta-galactosidase and not the endogenous mRNA. Beta galactosidase activity pattern mimic the endogenous gene expression pattern, with expression observed in the forebrain (dorsal horn). Mice homozygous for the mutation exhibit hyperalgesia, hypersensitive cutaneous and visceral nociception, loss of sensitivity to the analgesic effects of neuropeptide Y and resistance to barbiturates. Unlike wildtype mice, homozygotes fail to display capsaicin-induced neurogenic inflammatory responses. This mutant mouse strain may be useful in studies of the role of the neuropeptide Y receptor and the physiological effects of its ligand. | ||
| 002124 | C;129S-Ngfrtm1Jae/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ngfrtm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by 4 months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day 3, respectively. These ages coincide with the peak of naturally occurring cell death. | ||
| 002927 | CNCr.129P2-Cd40tm1Kik/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice exhibit impaired immunoglobulin class switching and germinal center formation. | ||
| 002267 | STOCK Bdnftm1Jae/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the Bdnftm1Jae mutation show about 1/2 normal levels of Bdnf mRNA, but appear normal. Mice homozygous for the Bdnftm1Jae mutation are smaller than normal siblings and most die within the second postnatal week. They have defective coordination of movements and balance. They also exhibit head bobbing and spinning during periods of hyperactivity. There are rare survivors to adulthood. There is excessive degeneration in all sensory ganglia examined, including the vestibular ganglion. Motor neurons are not affected. BDNF can prevent death of central motor neurons and other neurons in vitro, but does not affect these in vivo. | ||
| 003198 | STOCK Tg(huS100B)5Daoh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this transgene are viable and fertile. They have impaired learning and electrophysiological disturbances in the hippocampus. This strain may serve as a model of the mild learning impairment seen in human beings with Down syndrome (trisomy 21). | ||
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