Strain Name:

B6.129X1-Trpv1tm1Jul/J

Stock Number:

003770

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Mice that are homozygous for the targeted mutation, unlike wildtype mice, show no pain response and reduced swelling after subcutaneous hind paw injection of vanilloid compounds. They have a markedly attenuated response to acidified environments or heat (43 degrees C). 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.

Description

Strain Information

Former Names B6.129S4-Trpv1tm1Jul/J    (Changed: 18-OCT-05 )
B6.129S4-Vr1tm1Jul    (Changed: 15-DEC-04 )
Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.
Specieslaboratory mouse
GenerationN11F12 (17-SEP-12)
Generation Definitions
 
Donating InvestigatorDr. David Julius,   Univ of California at San Francisco

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Description
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.

Development
A targeting vector was used to disrupt an exon encoding part of the fifth and all of the sixth putative transmembrane domains together with the pore-loop region. The construct was electroporated into 129X1/SvJ-derived JM1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric animals were crossed to C57BL/6 female mice, and then backcrossed to the same for 10 generations.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Trpv1
017769   B6.129-Trpv1tm1(cre)Bbm/J
017623   B6.129-Trpv1tm2Bbm/J
View Strains carrying other alleles of Trpv1     (2 strains)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Trpv1tm1Jul/Trpv1tm1Jul

        B6.129X1-Trpv1tm1Jul/J
  • homeostasis/metabolism phenotype
  • abnormal physiological response to xenobiotic
    • anandamide-treated mice fail to exhibit phase I (decreased mean arterial blood pressure, cardiac contractility, and heart rate) and exhibit a reduced phase II pressor response compared with similarly treated wild-type mice   (MGI Ref ID J:105525)
    • capsaicin-treatment mice fail to exhibit a anandamide-like phase I and II response as in similarly treated wild-type mice   (MGI Ref ID J:105525)
    • however, the prolonged hypotensive response to anandamide-treatment is normal   (MGI Ref ID J:105525)
    • mice treated with PAR2-AP alone or in combination with capsaicin fail to exhibit thermal hyperalgesia unlike similarly treated wild-type mice   (MGI Ref ID J:96901)
    • mice fed a high fat diet and treated with capsaicin fail to exhibit a decrease in body weight compared with similarly treated wild-type mice   (MGI Ref ID J:133914)
    • following induction of colonic distention, mice fail to exhibit zymogen-induced behavioral hypersensitivity, as measured by visceral nociception, unlike similarly treated wild-type mice   (MGI Ref ID J:128319)
    • capsaicin-treated mice fail to exhibit synaptic depression unlike similarly treated wild-type mice   (MGI Ref ID J:132936)
    • 12-(S)-HPETE fails to depress synaptic transmission at excitatory synapses in interneurons unlike in wild-type mice   (MGI Ref ID J:132936)
  • altered response of heart to induced stress
    • after ischemia and during reperfusion, mice exhibit impaired recovery with lower left ventricular end diastolic pressure and higher left ventricle developed pressure and coronary flow compared with similarly treated wild-type mice   (MGI Ref ID J:116905)
    • however, treatment with calcitonin gene-related peptide or substance P improves postischemic recovery as in wild-type mice   (MGI Ref ID J:116905)
  • increased blood osmolality   (MGI Ref ID J:105254)
  • nervous system phenotype
  • abnormal nervous system electrophysiology
    • in response to hyperosmotic stimulation, supraoptic nucleus neurons fail to generate an increase in membrane conductance and depolarizing potentials unlike similarly treated wild-type cells   (MGI Ref ID J:105254)
    • abnormal action potential
      • impulse frequency of action potentials in colon sensory neurons at 45 degrees Celsius is lower than in similarly treated wild-type cells   (MGI Ref ID J:109767)
      • colon sensory neurons fail to exhibit a sustained-type current response to protons unlike similarly treated wild-type cells   (MGI Ref ID J:109767)
      • colon sensory neurons fail to exhibit a temperature sensitive response or 5-HT effect unlike similarly treated wild-type cells   (MGI Ref ID J:109767)
      • impaired ability to fire action potentials
        • temperatures below 50 degrees Celsius generate few action potentials in colon sensory neurons unlike in similarly treated wild-type cells   (MGI Ref ID J:109767)
  • abnormal neuronal precursor proliferation
    • neuronal precursor cell proliferation in the dorsal ganglion and subventricular zone (SVZ) is increased compared to in wild-type mice   (MGI Ref ID J:102006)
    • SR141716A does not affected proliferation in the dorsal ganglion and decreases proliferation in the SVZ unlike in similarly treated wild-type mice   (MGI Ref ID J:102006)
  • decreased synaptic depression
    • capsaicin-treated mice fail to exhibit synaptic depression unlike similarly treated wild-type mice   (MGI Ref ID J:132936)
    • 12-(S)-HPETE fails to depress synaptic transmission at excitatory synapses in interneurons unlike in wild-type mice   (MGI Ref ID J:132936)
  • reduced long term depression   (MGI Ref ID J:132936)
  • cardiovascular system phenotype
  • altered response of heart to induced stress
    • after ischemia and during reperfusion, mice exhibit impaired recovery with lower left ventricular end diastolic pressure and higher left ventricle developed pressure and coronary flow compared with similarly treated wild-type mice   (MGI Ref ID J:116905)
    • however, treatment with calcitonin gene-related peptide or substance P improves postischemic recovery as in wild-type mice   (MGI Ref ID J:116905)
  • decreased left ventricle diastolic pressure
    • after ischemia and during reperfusion   (MGI Ref ID J:116905)
  • increased coronary flow rate
    • after ischemia and during reperfusion   (MGI Ref ID J:116905)
  • increased left ventricle developed pressure
    • after ischemia and during reperfusion   (MGI Ref ID J:116905)
  • growth/size/body phenotype
  • increased body weight
    • mice fed a high fat diet and treated with capsaicin fail to exhibit a decrease in body weight compared with similarly treated wild-type mice   (MGI Ref ID J:133914)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • mice exhibit normal tactile hypersensitivity and allodynia following spinal nerve ligation   (MGI Ref ID J:132700)
    • mice exhibit normal water consumption and ethanol-induced conditioned taste aversion   (MGI Ref ID J:153529)
    • abnormal mechanical nociception
      • following induction of colonic distention, mice fail to exhibit zymogen-induced behavioral hypersensitivity, as measured by visceral nociception, unlike similarly treated wild-type mice   (MGI Ref ID J:128319)
    • alcohol preference
      • mice exhibit greater preference for ethanol than wild type mice in a two-bottle test   (MGI Ref ID J:153529)
    • altered righting response
      • duration of loss of righting reflex following ethanol consumption (at 3.2 g/kg and 3.4 g/kg but not 3.8 g/kg) is shorter than in similarly treated wild-type mice   (MGI Ref ID J:153529)
    • impaired behavioral response to alcohol
      • duration of loss of righting reflex following ethanol consumption (at 3.2 g/kg and 3.4 g/kg but not 3.8 g/kg) is shorter than in similarly treated wild-type mice   (MGI Ref ID J:153529)
      • recovery from impaired coordination following ethanol consumption is faster than for similarly treated wild-type mice   (MGI Ref ID J:153529)
      • however, mice exhibit normal acute ethanol withdrawal severity   (MGI Ref ID J:153529)
    • impaired coordination
      • recovery from impaired coordination following ethanol consumption is faster than for similarly treated wild-type mice   (MGI Ref ID J:153529)
    • increased alcohol consumption
      • mice consume more ethanol than wild-type mice in a two-bottle test   (MGI Ref ID J:153529)
    • increased thermal nociceptive threshold
      • mice treated with PAR2-AP alone or in combination with capsaicin fail to exhibit thermal hyperalgesia unlike similarly treated wild-type mice   (MGI Ref ID J:96901)
  • taste/olfaction phenotype
  • abnormal taste sensitivity
    • at high concentrations, mice exhibit a less aversion to FeSO4 than wild-type mice   (MGI Ref ID J:145940)
    • mice exhibit less aversion to 10 mM CuSO4 than wild-type mice   (MGI Ref ID J:145940)
    • however, aversion to ZnSO4 is normal   (MGI Ref ID J:145940)
  • integument phenotype
  • abnormal hair cycle
    • mice exhibit delays in the onset of catagen and telogen compared with wild-type mice   (MGI Ref ID J:110694)
    • however, follicle cycling is normal once initiated   (MGI Ref ID J:110694)
    • abnormal hair cycle catagen phase
      • at P19, mice exhibit a retardation in catagen compared with wild-type mice   (MGI Ref ID J:110694)
    • abnormal hair cycle telogen phase
      • slightly retarded at P25   (MGI Ref ID J:110694)
  • abnormal mechanical nociception
    • following induction of colonic distention, mice fail to exhibit zymogen-induced behavioral hypersensitivity, as measured by visceral nociception, unlike similarly treated wild-type mice   (MGI Ref ID J:128319)
  • increased thermal nociceptive threshold
    • mice treated with PAR2-AP alone or in combination with capsaicin fail to exhibit thermal hyperalgesia unlike similarly treated wild-type mice   (MGI Ref ID J:96901)
  • cellular phenotype
  • abnormal neuronal precursor proliferation
    • neuronal precursor cell proliferation in the dorsal ganglion and subventricular zone (SVZ) is increased compared to in wild-type mice   (MGI Ref ID J:102006)
    • SR141716A does not affected proliferation in the dorsal ganglion and decreases proliferation in the SVZ unlike in similarly treated wild-type mice   (MGI Ref ID J:102006)

Trpv1tm1Jul/Trpv1tm1Jul

        B6.129X1-Trpv1tm1Jul
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • mice exhibit normal general locomotion and pain threshold   (MGI Ref ID J:117778)
    • abnormal behavior
      • mice exhibit less freezing after stress sensitization compared with wild-type mice   (MGI Ref ID J:117778)
      • decreased anxiety-related response
        • in a light-dark test, mice spend more time exploring the light compartment than wild-type mice   (MGI Ref ID J:117778)
        • in an elevated plus maze, mice spend more time in open arms and make more entries into open arms compared with wild-type mice   (MGI Ref ID J:117778)
      • impaired contextual conditioning behavior
        • mice exhibit less conditioned freezing in response to a context compared with wild-type mice   (MGI Ref ID J:117778)
      • impaired cued conditioning behavior
        • mice exhibit less conditioned freezing in response to an auditory cue compared with wild-type mice   (MGI Ref ID J:117778)
  • renal/urinary system phenotype
  • abnormal renal tubule morphology
    • DOCA-salt-treated mice exhibit more severe renal tubular injury in the renal cortex and outer medulla than similarly treated wild-type mice   (MGI Ref ID J:154624)
    • however, DEXA treatment reduces renal tubule damage   (MGI Ref ID J:154624)
  • abnormal urine homeostasis
    • DOCA-salt-treated mice exhibit a greater increase in urinary 8-isoprostane and albumin excretion compared with similarly treated wild-type mice   (MGI Ref ID J:154624)
    • however, DEXA treatment decreased urinary 8-isoprotane and albumin excretion   (MGI Ref ID J:154624)
    • increased urine protein level
      • DOCA-salt-treated mice exhibit a greater increase in urinary albumin excretion compared with similarly treated wild-type mice   (MGI Ref ID J:154624)
      • however, DEXA treatment decreased urinary albumin excretion   (MGI Ref ID J:154624)
  • glomerulosclerosis
    • DOCA-salt-treated mice exhibit a greater glomerulosclerosis than similarly treated wild-type mice   (MGI Ref ID J:154624)
    • however, DEXA treatment reduces glomerulosclerosis   (MGI Ref ID J:154624)
  • kidney inflammation
    • DOCA-salt-treated mice exhibit a more monocyte/macrophage and CD3+ T cell infiltration than similarly treated wild-type mice   (MGI Ref ID J:154624)
    • however, DEXA treatment prevents kidney inflammation   (MGI Ref ID J:154624)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • mice exhibit normal paired-pulse facilitation, auditory brainstem responses, and distortion-product otoacoustic emissions   (MGI Ref ID J:117778)
    • reduced long term potentiation
      • following high frequency stimulation, long term potentiation is weaker than in similarly treated wild-type mice   (MGI Ref ID J:117778)
  • homeostasis/metabolism phenotype
  • abnormal urine homeostasis
    • DOCA-salt-treated mice exhibit a greater increase in urinary 8-isoprostane and albumin excretion compared with similarly treated wild-type mice   (MGI Ref ID J:154624)
    • however, DEXA treatment decreased urinary 8-isoprotane and albumin excretion   (MGI Ref ID J:154624)
    • increased urine protein level
      • DOCA-salt-treated mice exhibit a greater increase in urinary albumin excretion compared with similarly treated wild-type mice   (MGI Ref ID J:154624)
      • however, DEXA treatment decreased urinary albumin excretion   (MGI Ref ID J:154624)
  • increased susceptibility to injury
    • DOCA-salt-treated mice exhibit increased renal damage compared with similarly treated wild-type mice   (MGI Ref ID J:154624)
    • however, DEXA treatment ameliorates renal damage   (MGI Ref ID J:154624)
  • immune system phenotype
  • abnormal chemokine secretion
    • DOCA-salt-treated mice exhibit increased MCP-1 protein levels in the kidneys of compared with similarly treated wild-type mice   (MGI Ref ID J:154624)
    • however, DEXA treatment restores normal levels   (MGI Ref ID J:154624)
  • increased interleukin-6 secretion
    • DOCA-salt-treated mice exhibit increased IL6 protein levels in the kidneys of compared with similarly treated wild-type mice   (MGI Ref ID J:154624)
    • however, DEXA treatment restores normal levels   (MGI Ref ID J:154624)
  • increased tumor necrosis factor secretion
    • DOCA-salt-treated mice exhibit increased TNFalpha protein levels in the kidneys of compared with similarly treated wild-type mice   (MGI Ref ID J:154624)
    • however, DEXA treatment restores normal levels   (MGI Ref ID J:154624)
  • kidney inflammation
    • DOCA-salt-treated mice exhibit a more monocyte/macrophage and CD3+ T cell infiltration than similarly treated wild-type mice   (MGI Ref ID J:154624)
    • however, DEXA treatment prevents kidney inflammation   (MGI Ref ID J:154624)

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Trpv1tm1Jul/Trpv1tm1Jul

        involves: 129X1/SvJ
  • behavior/neurological phenotype
  • abnormal nociception after inflammation
    • reduced thermal hypersensitvitiy following inflammation   (MGI Ref ID J:61534)
  • decreased fluid intake
    • following an injection of a hypertonic solution, mice drink water less than similarly treated wild-type mice   (MGI Ref ID J:112194)
  • hypoalgesia
    • mutants show normal responses to noxious mechanical stimuli but exhibit no vanilloid-evoked pain behavior, are impaired in the detection of painful heat, and show little thermal hypersensitivity in the setting of inflammation   (MGI Ref ID J:61534)
    • cheek injection of capsaicin does not evoke pain behavior (forepaw facial wiping), in contrast to robust facial wiping observed in treated wild-type   (MGI Ref ID J:197482)
    • increased chemical nociceptive threshold
      • mutants exhibit no vanilloid (capsaicin and resiniferatoxin) evoked pain behavior: no behavioral response and less swelling with vanilloid injection into plantar skin of hind paw, no aversive response to drinking capsaicin supplemented water, and no reduction in temperature in response to capsaicin injection   (MGI Ref ID J:61534)
    • increased thermal nociceptive threshold
      • mutants exhibit reduced sensitivity to painful heat in behavioral tests, with longer mean withdrawal latencies in the tail immersion test at temperatures greater than 48 degrees Celcius and longer response latencies at temperatures greater than 50 degrees Celcius in the hot plate assay   (MGI Ref ID J:61534)
      • mutants treated with mustard oil show little or no change in hot plate latency   (MGI Ref ID J:61534)
      • mice show increased latencies (impaired nociceptive response) in tail-immersion and hot plate paradigms   (MGI Ref ID J:197482)
  • nervous system phenotype
  • abnormal nervous system electrophysiology
    • in response to osmotic stimulation, organum vasculosum lamina terminalis neurons fail to exhibit changes in membrane potential or conductance unlike similarly treated wild-type cells   (MGI Ref ID J:112194)
    • impaired ability to fire action potentials
      • in response to osmotic stimulation, organum vasculosum lamina terminalis neurons fail to exhibit an increase in action potential firing compared with similarly treated wild-type cells   (MGI Ref ID J:112194)
  • abnormal sensory neuron physiology
    • sensory neurons and primary afferent fibers show a reduction in proton (pH5) sensitivity in vitro (acid-evoked nociception)   (MGI Ref ID J:61534)
    • incidence of noxious heat-evoked currents of the moderate-threshold (greater than 43 degrees Celcius) class is reduced in cultured sensory neurons or sensory nerve fibers but high-threshold responses remain intact   (MGI Ref ID J:61534)
    • vanilloid compounds, capsaicin and resiniferatoxin, are completely inactive on neurons from mutants, showing no increases in calcium or inward currents   (MGI Ref ID J:61534)
    • mutants treated with mustard oil show little or no chmutants treated with mustard oil show no enhancement of thermally evoked responses in wide dynamic range neurons of the lumbar dorsal horn   (MGI Ref ID J:61534)
  • adipose tissue phenotype
  • decreased abdominal fat pad weight
    • when fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:137026)
  • decreased fat cell size
    • when fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:137026)
  • decreased subcutaneous adipose tissue amount
    • when fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:137026)
  • growth/size/body phenotype
  • decreased susceptibility to diet-induced obesity
    • when fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:137026)
  • homeostasis/metabolism phenotype
  • abnormal adaptive thermogenesis
    • whether fed a standard or high fat diet, cold-treated mice do not exhibit the drop in body temperature observed in similarly treated wild-type mice   (MGI Ref ID J:137026)
  • decreased susceptibility to diet-induced obesity
    • when fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:137026)
  • liver/biliary system phenotype
  • decreased susceptibility to hepatic steatosis
    • when fed a high fat diet, mice exhibit reduced hepatic fat content and reduced lipid droplets compared with similarly treated wild-type mice   (MGI Ref ID J:137026)
  • integument phenotype
  • abnormal nociception after inflammation
    • reduced thermal hypersensitvitiy following inflammation   (MGI Ref ID J:61534)
  • decreased subcutaneous adipose tissue amount
    • when fed a high fat diet compared with similarly treated wild-type mice   (MGI Ref ID J:137026)
  • hypoalgesia
    • mutants show normal responses to noxious mechanical stimuli but exhibit no vanilloid-evoked pain behavior, are impaired in the detection of painful heat, and show little thermal hypersensitivity in the setting of inflammation   (MGI Ref ID J:61534)
    • cheek injection of capsaicin does not evoke pain behavior (forepaw facial wiping), in contrast to robust facial wiping observed in treated wild-type   (MGI Ref ID J:197482)
    • increased chemical nociceptive threshold
      • mutants exhibit no vanilloid (capsaicin and resiniferatoxin) evoked pain behavior: no behavioral response and less swelling with vanilloid injection into plantar skin of hind paw, no aversive response to drinking capsaicin supplemented water, and no reduction in temperature in response to capsaicin injection   (MGI Ref ID J:61534)
    • increased thermal nociceptive threshold
      • mutants exhibit reduced sensitivity to painful heat in behavioral tests, with longer mean withdrawal latencies in the tail immersion test at temperatures greater than 48 degrees Celcius and longer response latencies at temperatures greater than 50 degrees Celcius in the hot plate assay   (MGI Ref ID J:61534)
      • mutants treated with mustard oil show little or no change in hot plate latency   (MGI Ref ID J:61534)
      • mice show increased latencies (impaired nociceptive response) in tail-immersion and hot plate paradigms   (MGI Ref ID J:197482)

Trpv1tm1Jul/Trpv1tm1Jul

        involves: 129X1/SvJ * C57BL/6
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • mice exhibit normal circadian core body temperature, response to warm or cold exposure, and ethanol-induced hypothermia   (MGI Ref ID J:104828)
    • impaired febrile response
      • the amplitude of the fever response to LPS-treatment is blunted compared to in similarly treated wild-type mice   (MGI Ref ID J:104828)
    • increased incidence of tumors by chemical induction
      • skin carcinogenesis is enhanced in mice treated with DMBA and TPA over a period of 21 weeks   (MGI Ref ID J:144978)
      • about 75% of mice developed skin tumors compared to under 25% for controls, with the tumors being larger and more numerous   (MGI Ref ID J:144978)
  • renal/urinary system phenotype
  • abnormal urination
    • increased frequency of non-voiding contractions   (MGI Ref ID J:78707)
    • the frequency of and strength voiding contractions were similar those of wild-type littermates   (MGI Ref ID J:78707)
  • tumorigenesis
  • increased incidence of tumors by chemical induction
    • skin carcinogenesis is enhanced in mice treated with DMBA and TPA over a period of 21 weeks   (MGI Ref ID J:144978)
    • about 75% of mice developed skin tumors compared to under 25% for controls, with the tumors being larger and more numerous   (MGI Ref ID J:144978)
  • immune system phenotype
  • decreased susceptibility to endotoxin shock
    • the amplitude of the fever response to LPS-treatment is blunted compared to in similarly treated wild-type mice   (MGI Ref ID J:104828)
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Research Applications
This mouse can be used to support research in many areas including:

Trpv1tm1Jul related

Immunology, Inflammation and Autoimmunity Research
Inflammation

Neurobiology Research
Receptor Defects

Sensorineural Research
Nociception

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Trpv1tm1Jul
Allele Name targeted mutation 1, David Julius
Allele Type Targeted (knock-out)
Common Name(s) TRPV1-KO; Trpv-1-; Vr1tm1Jul;
Mutation Made ByDr. David Julius,   Univ of California at San Francisco
Strain of Origin129X1/SvJ
ES Cell Line NameJM-1
ES Cell Line Strain129X1/SvJ
Gene Symbol and Name Trpv1, transient receptor potential cation channel, subfamily V, member 1
Chromosome 11
Gene Common Name(s) OTRPC1; VR-1; VR.5'sv; VR1; Vr1; Vr1l1; capsaicin receptor; vanilloid receptor subtype 1;
Molecular Note The gene was disrupted by deleting an exon encoding part of the fifth and all of the sixth putative transmembrane domains of the channel, together with the intervening pore-loop region. Northern blot analysis showed that mRNA derived from dorsal root ganglia (DRG) of homozygous mice lacked detectable transcripts encoded by this allele. [MGI Ref ID J:61534]

Genotyping

Genotyping Information

Genotyping Protocols

NntC57BL/6J,

Separated MCA


Trpv1tm1Jul, Separated PCR
Trpv1tm1Jul, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Caterina MJ; Leffler A; Malmberg AB; Martin WJ; Trafton J; Petersen-Zeitz KR; Koltzenburg M; Basbaum AI; Julius D. 2000. Impaired nociception and pain sensation in mice lacking the capsaicin receptor [see comments] Science 288(5464):306-13. [PubMed: 10764638]  [MGI Ref ID J:61534]

Additional References

Alter BJ; Gereau RW 4th. 2008. Hotheaded: TRPV1 as Mediator of Hippocampal Synaptic Plasticity. Neuron 57(5):629-31. [PubMed: 18341983]  [MGI Ref ID J:131803]

Trpv1tm1Jul related

Ahern GP; Brooks IM; Miyares RL; Wang XB. 2005. Extracellular cations sensitize and gate capsaicin receptor TRPV1 modulating pain signaling. J Neurosci 25(21):5109-16. [PubMed: 15917451]  [MGI Ref ID J:98540]

Akopian AN; Ruparel NB; Jeske NA; Hargreaves KM. 2007. Transient receptor potential TRPA1 channel desensitization in sensory neurons is agonist dependent and regulated by TRPV1-directed internalization. J Physiol 583(Pt 1):175-93. [PubMed: 17584831]  [MGI Ref ID J:140830]

Alter BJ; Gereau RW 4th. 2008. Hotheaded: TRPV1 as Mediator of Hippocampal Synaptic Plasticity. Neuron 57(5):629-31. [PubMed: 18341983]  [MGI Ref ID J:131803]

Amadesi S; Nie J; Vergnolle N; Cottrell GS; Grady EF; Trevisani M; Manni C; Geppetti P; McRoberts JA; Ennes H; Davis JB; Mayer EA; Bunnett NW. 2004. Protease-activated receptor 2 sensitizes the capsaicin receptor transient receptor potential vanilloid receptor 1 to induce hyperalgesia. J Neurosci 24(18):4300-12. [PubMed: 15128844]  [MGI Ref ID J:96901]

Andersson DA; Gentry C; Bevan S. 2012. TRPA1 has a key role in the somatic pro-nociceptive actions of hydrogen sulfide. PLoS One 7(10):e46917. [PubMed: 23071662]  [MGI Ref ID J:192090]

Baiou D; Santha P; Avelino A; Charrua A; Bacskai T; Matesz K; Cruz F; Nagy I. 2007. Neurochemical characterization of insulin receptor-expressing primary sensory neurons in wild-type and vanilloid type 1 transient receptor potential receptor knockout mice. J Comp Neurol 503(2):334-47. [PubMed: 17492627]  [MGI Ref ID J:132840]

Bautista DM; Sigal YM; Milstein AD; Garrison JL; Zorn JA; Tsuruda PR; Nicoll RA; Julius D. 2008. Pungent agents from Szechuan peppers excite sensory neurons by inhibiting two-pore potassium channels. Nat Neurosci 11(7):772-9. [PubMed: 18568022]  [MGI Ref ID J:139352]

Bavassano C; Marvaldi L; Langeslag M; Sarg B; Lindner H; Klimaschewski L; Kress M; Ferrer-Montiel A; Knaus HG. 2013. Identification of voltage-gated K(+) channel beta 2 (Kvbeta2) subunit as a novel interaction partner of the pain transducer Transient Receptor Potential Vanilloid 1 channel (TRPV1). Biochim Biophys Acta 1833(12):3166-75. [PubMed: 24036102]  [MGI Ref ID J:204072]

Bielefeldt K; Davis BM. 2008. Differential effects of ASIC3 and TRPV1 deletion on gastroesophageal sensation in mice. Am J Physiol Gastrointest Liver Physiol 294(1):G130-8. [PubMed: 17975130]  [MGI Ref ID J:130510]

Birder LA; Nakamura Y; Kiss S; Nealen ML; Barrick S; Kanai AJ; Wang E; Ruiz G; De Groat WC; Apodaca G; Watkins S; Caterina MJ. 2002. Altered urinary bladder function in mice lacking the vanilloid receptor TRPV1. Nat Neurosci 5(9):856-60. [PubMed: 12161756]  [MGI Ref ID J:78707]

Biro T; Bodo E; Telek A; Geczy T; Tychsen B; Kovacs L; Paus R. 2006. Hair cycle control by vanilloid receptor-1 (TRPV1): evidence from TRPV1 knockout mice. J Invest Dermatol 126(8):1909-12. [PubMed: 16645591]  [MGI Ref ID J:110694]

Blednov YA; Harris RA. 2009. Deletion of vanilloid receptor (TRPV1) in mice alters behavioral effects of ethanol. Neuropharmacology 56(4):814-20. [PubMed: 19705551]  [MGI Ref ID J:153529]

Bode AM; Cho YY; Zheng D; Zhu F; Ericson ME; Ma WY; Yao K; Dong Z. 2009. Transient receptor potential type vanilloid 1 suppresses skin carcinogenesis. Cancer Res 69(3):905-13. [PubMed: 19155296]  [MGI Ref ID J:144978]

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Treesukosol Y; Lyall V; Heck GL; Desimone JA; Spector AC. 2007. A psychophysical and electrophysiological analysis of salt taste in Trpv1 null mice. Am J Physiol Regul Integr Comp Physiol 292(5):R1799-809. [PubMed: 17234959]  [MGI Ref ID J:121472]

Vinuesa AG; Sancho R; Garcia-Limones C; Behrens A; ten Dijke P; Calzado MA; Munoz E. 2012. Vanilloid receptor-1 regulates neurogenic inflammation in colon and protects mice from colon cancer. Cancer Res 72(7):1705-16. [PubMed: 22396497]  [MGI Ref ID J:184884]

Vriens J; Owsianik G; Hofmann T; Philipp SE; Stab J; Chen X; Benoit M; Xue F; Janssens A; Kerselaers S; Oberwinkler J; Vennekens R; Gudermann T; Nilius B; Voets T. 2011. TRPM3 is a nociceptor channel involved in the detection of noxious heat. Neuron 70(3):482-94. [PubMed: 21555074]  [MGI Ref ID J:174798]

Wang L; Wang DH. 2005. TRPV1 gene knockout impairs postischemic recovery in isolated perfused heart in mice. Circulation 112(23):3617-23. [PubMed: 16314376]  [MGI Ref ID J:116905]

Wang Y; Wang DH. 2009. Aggravated renal inflammatory responses in TRPV1 gene knockout mice subjected to DOCA-salt hypertension. Am J Physiol Renal Physiol 297(6):F1550-9. [PubMed: 19794112]  [MGI Ref ID J:154624]

Woodbury CJ; Zwick M; Wang S; Lawson JJ; Caterina MJ; Koltzenburg M; Albers KM; Koerber HR; Davis BM. 2004. Nociceptors lacking TRPV1 and TRPV2 have normal heat responses. J Neurosci 24(28):6410-5. [PubMed: 15254097]  [MGI Ref ID J:144159]

Xu ZZ; Zhang L; Liu T; Park JY; Berta T; Yang R; Serhan CN; Ji RR. 2010. Resolvins RvE1 and RvD1 attenuate inflammatory pain via central and peripheral actions. Nat Med 16(5):592-7, 1p following 597. [PubMed: 20383154]  [MGI Ref ID J:161538]

Yamada T; Ugawa S; Ueda T; Ishida Y; Kajita K; Shimada S. 2009. Differential localizations of the transient receptor potential channels TRPV4 and TRPV1 in the mouse urinary bladder. J Histochem Cytochem 57(3):277-87. [PubMed: 19029406]  [MGI Ref ID J:146943]

Yang D; Luo Z; Ma S; Wong WT; Ma L; Zhong J; He H; Zhao Z; Cao T; Yan Z; Liu D; Arendshorst WJ; Huang Y; Tepel M; Zhu Z. 2010. Activation of TRPV1 by dietary capsaicin improves endothelium-dependent vasorelaxation and prevents hypertension. Cell Metab 12(2):130-41. [PubMed: 20674858]  [MGI Ref ID J:163079]

Yin S; Luo J; Qian A; Du J; Yang Q; Zhou S; Yu W; Du G; Clark RB; Walters ET; Carlton SM; Hu H. 2013. Retinoids activate the irritant receptor TRPV1 and produce sensory hypersensitivity. J Clin Invest 123(9):3941-51. [PubMed: 23925292]  [MGI Ref ID J:201619]

Zhang LL; Yan Liu D; Ma LQ; Luo ZD; Cao TB; Zhong J; Yan ZC; Wang LJ; Zhao ZG; Zhu SJ; Schrader M; Thilo F; Zhu ZM; Tepel M. 2007. Activation of transient receptor potential vanilloid type-1 channel prevents adipogenesis and obesity. Circ Res 100(7):1063-70. [PubMed: 17347480]  [MGI Ref ID J:133914]

Zhong B; Wang DH. 2008. N-oleoyldopamine, a novel endogenous capsaicin-like lipid, protects the heart against ischemia-reperfusion injury via activation of TRPV1. Am J Physiol Heart Circ Physiol 295(2):H728-35. [PubMed: 18567714]  [MGI Ref ID J:138221]

Zhong B; Wang DH. 2007. TRPV1 gene knockout impairs preconditioning protection against myocardial injury in isolated perfused hearts in mice. Am J Physiol Heart Circ Physiol 293(3):H1791-8. [PubMed: 17586621]  [MGI Ref ID J:126121]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX8

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice are bred as homozygotes. Coat color expected from breeding:Black
Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $130.00Female or MaleHomozygous for Trpv1tm1Jul  
4 weeks $130.00Female or MaleHomozygous for Trpv1tm1Jul  
5 weeks $130.00Female or MaleHomozygous for Trpv1tm1Jul  
6 weeks $135.25Female or MaleHomozygous for Trpv1tm1Jul  
7 weeks $140.50Female or MaleHomozygous for Trpv1tm1Jul  
8 weeks $145.75Female or MaleHomozygous for Trpv1tm1Jul  
9 weeks $151.00Female or MaleHomozygous for Trpv1tm1Jul  
10 weeks $156.25Female or MaleHomozygous for Trpv1tm1Jul  
11 weeks $161.50Female or MaleHomozygous for Trpv1tm1Jul  
12 weeks $166.75Female or MaleHomozygous for Trpv1tm1Jul  
Price per Pair (US dollars $)Pair Genotype
$270.50Homozygous for Trpv1tm1Jul x Homozygous for Trpv1tm1Jul  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $169.00Female or MaleHomozygous for Trpv1tm1Jul  
4 weeks $169.00Female or MaleHomozygous for Trpv1tm1Jul  
5 weeks $169.00Female or MaleHomozygous for Trpv1tm1Jul  
6 weeks $175.90Female or MaleHomozygous for Trpv1tm1Jul  
7 weeks $182.70Female or MaleHomozygous for Trpv1tm1Jul  
8 weeks $189.50Female or MaleHomozygous for Trpv1tm1Jul  
9 weeks $196.30Female or MaleHomozygous for Trpv1tm1Jul  
10 weeks $203.20Female or MaleHomozygous for Trpv1tm1Jul  
11 weeks $210.00Female or MaleHomozygous for Trpv1tm1Jul  
12 weeks $216.80Female or MaleHomozygous for Trpv1tm1Jul  
Price per Pair (US dollars $)Pair Genotype
$351.70Homozygous for Trpv1tm1Jul x Homozygous for Trpv1tm1Jul  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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