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- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
Description
The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.
Strain Information
Former Names B6C3Fe a/a- anx/J (Changed: 15-DEC-04 ) B6C3Fe-a/a-anx (Changed: 15-DEC-04 ) Type Mutant Strain; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Generation N28 F1 Appearance
black, affected
Related Genotype: a anx/a anx
black, unaffected
Related Genotype: a ?/a +Description
Compared with their wildtype siblings, anx/anx homozygotes are characterized by a thinning in the neck and tail at 5 days of age, lower body weight detectable by 9 days of age, and death by 22 days of age on the B6C3H-a/a background. Outbreeding to CAST/Ei modifies the phenotype such that homozygotes live to approximately 5 weeks of age. Evaluation of stomach content shows that anx/anx mice ingest less than their siblings. They show headweaving, body tremors, uncoordinated gait, and hyperactivity along with diminished adipose tissue and reduced serum leptin levels. (Maltais et al., 1984; Johansen et al., 2000)Intraperitoneal injection of 20 day old pups with 5,7-dihydroxytryptamine, a seratonin antagonist, reduces the severity of the neurological phenotypes. Homozygotes have extensive serotonergic hyperinnervation in normal target fields including the hippocampus, frontal cortex, olfactory bulb, and cerebellum, yet they have normal catecholaminergic innervation. This hyperinnervation is thought to reflect increased arborization of axonal fibers since there is no increase in serotonergic cell bodies. In the raphe nuiclues, there are decreased mRNA levels of serotonin transp orter (Slc6a4 previously Htt or 5-Htt) and tryptophan hydroxylase activity is diminished. Similar to food deprived wild type mice, anx/anx mice show decreased mRNA of monoamine oxidase A in the locus ceruleus but not the raphe nuclei. (Maltais et al., 1984; Son et al., 1994; Jahng et al., 1998, Brain Res; Jahng et al., 1998, Dev Brain Res.)
Despite their failure to eat adequately, homozygotes do not show elevated neuropeptide Y mRNA levels in the hypothalamic arcuate nucleus. However, immunohistochemistry revealed increased perikaryal neuropeptide Y staining in the arcuate nucleus and decreased density and neuropeptide Y staining of neuropeptide Y terminals in the paraventricular, arcuate, and other hypothalamic nuclei. Neuropeptide Y staining in the suprachiasmatic and thalamic paraventricular nuclei is normal. There is a similarly altered pattern of expression for agouti gene-related protein with immunoreacitvity increased in the cell body and decreased in the terminals in arcuate neurons despite apparently normal mRNA levels. (Broberger et al., 1997; Jahng et al., 1998, Brain Res; Broberger at el., 1998)
The arcuate nucleus also has a reduction in the number of pro-opiomelanocortin expressing neurons, a reduction in mRNA levels of pro-opiomelanocor tin and neuropeptide Y receptors Y1 and Y5, and a reduction in immunoreactivity of neuropeptide Y receptor Y2, adrenocorticotropic hormone, and alpha melanocyte stimulating hormone. Decreased staining of aspartate, acetylcholinesterase, and somatostatin was also seen in the arcuate nucleus. Decreased staining of cocaine and amphetamine regulated transcript in the arcuate nucleus and other regions of the hyopthalamus has also been reported. This pattern of decreased staining of pro-opiomelanocortin neurons may be due to degeneration of this cell population. No changes in brain cholecystokinin, galanin, or serotonin were detected by immunohistochemistry. (Broberger et al., 1997; Broberger et al., 1999; Johansen et al., 2000.)
The dentate gyrus of anx/anx mice is smaller than normal and has an increase in both the number of proliferating cells and cells undergoing apoptosis according to BrdU and TUNEL assessment. (Kim et al., 2001.)
Control Information
| Control | ||
|---|---|---|
| Untyped from the colony | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying a allele
View Strains carrying a (104 strains)
Phenotype
Phenotype Information
assigned by genotype
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
anx/anx
B6C3Fe a/a-anx/J
- life span-post-weaning/aging
- premature death (MGI Ref ID J:7689)
- mutant mice die in a state of anorexia and emaciation at ~P22
- behavior/neurological phenotype
- abnormal eating behavior (MGI Ref ID J:7689)
- failure to ingest sufficient amount of nutrients to sustain growth, indicating anorexia, starting at ~P5
- however, no deficiency in dietary or serum zinc (a frequent metabolic cause of anorexia) is observed
- abnormal suckling behavior (MGI Ref ID J:7689)
- physiological and behavioral phenotypes appear to result from a suckling dysfunction
- abnormal gait (MGI Ref ID J:7689)
- uncoordinated gait at P18 or later
- reduction in severity of abnormal gait following i.p. injection of the serotonin antagonist 5,7-dihydroxytryptamine at P20
- abnormal head movements (MGI Ref ID J:7689)
- headweaving at P18 or later
- hyperactivity (MGI Ref ID J:7689)
- hyperactivity at P18 or later
- reduction in hyperactivity following i.p. injection of the serotonin antagonist 5,7-dihydroxytryptamine at P20
- tremors (MGI Ref ID J:7689)
- head and body tremors at P18 or later
- reduction in severity of head and body tremors following i.p. injection of the serotonin antagonist 5,7-dihydroxytryptamine at P20
- growth/size phenotype
- decreased body weight (MGI Ref ID J:7689)
- significant reduction in body weight at P9
- cachexia (MGI Ref ID J:7689)
- anorexic mutants are first recognized at ~P5 by a thinning of the neck and tail, and later by growth arrest and emaciation
- immune system phenotype
- abnormal inflammatory response (MGI Ref ID J:103396)
- increased thymus weight (MGI Ref ID J:7689)
- significant increase in thymus weight at P15 but not at P5
- pale spleen (MGI Ref ID J:7689)
- beginning at ~P5, spleen is pale in color
- however, total RBC count, hemoglobin, hematocrit, and mean corpuscular volume (MCV) are within normal range
- small spleen (MGI Ref ID J:7689)
- beginning at ~P5, spleen size is reduced
- decreased spleen weight (MGI Ref ID J:7689)
- significant reduction in spleen weight both at P5 and at P15
- homeostasis/metabolism phenotype
- decreased body temperature (MGI Ref ID J:7689)
- significant hypothermia at ~P22, but not at P5, P10 or P15
- hypoglycemia (MGI Ref ID J:7689)
- significantly decreased blood glucose levels relative to wild-type littermates at P15 (58 mg/dl vs 129 mg/dl, respectively)
- increased blood urea nitrogen level (MGI Ref ID J:7689)
- significantly increased blood urea nitrogen levels relative to wild-type littermates at P15 (62.5 mg/dl vs 43.8 mg/dl, respectively)
- increased blood uric acid level (MGI Ref ID J:7689)
- significantly increased blood uric acid levels relative to wild-type littermates at P15 (4.6 mg/dl vs 1.2 mg/dl, respectively)
- increased circulating alkaline phosphatase level (MGI Ref ID J:7689)
- significantly increased circulating alkaline phosphatase levels relative to wild-type littermates at P15 (1020 mU/ml vs 385 mU/ml, respectively)
- increased circulating cholesterol level (MGI Ref ID J:7689)
- significantly increased serum cholesterol levels relative to wild-type littermates at P15 (1.92 ± 0.18 mg/ml vs 1.12 ± 0.04 mg/ml, respectively)
- liver/biliary system phenotype
- abnormal liver morphology (MGI Ref ID J:7689)
- at P15, livers display a lacey appearance and are devoid of fat and glycogen
- nervous system phenotype
- abnormal brain vasculature (MGI Ref ID J:7689)
- at P15, brains display an abundance of capillaries
- increased brain weight (MGI Ref ID J:7689)
- significant increase in brain weight both at P5 and at P15
- cardiovascular system phenotype
- abnormal brain vasculature (MGI Ref ID J:7689)
- at P15, brains display an abundance of capillaries
- hematopoietic system phenotype
- increased thymus weight (MGI Ref ID J:7689)
- significant increase in thymus weight at P15 but not at P5
- pale spleen (MGI Ref ID J:7689)
- beginning at ~P5, spleen is pale in color
- however, total RBC count, hemoglobin, hematocrit, and mean corpuscular volume (MCV) are within normal range
- small spleen (MGI Ref ID J:7689)
- beginning at ~P5, spleen size is reduced
- decreased spleen weight (MGI Ref ID J:7689)
- significant reduction in spleen weight both at P5 and at P15
anx/anx
involves: DW/J * M. m. domesticus poschiavinus * Swiss
- life span-post-weaning/aging
- premature death (MGI Ref ID J:13936)
- mutant mice die in a state of anorexia and emaciation at ~P22
- behavior/neurological phenotype
- abnormal gait (MGI Ref ID J:13936)
- uncoordinated gait
- decreased eating behavior (MGI Ref ID J:13936)
- poor appetite starting at ~P5
- failure to ingest sufficient amount of nutrients to sustain growth, indicating anorexia
- hyperactivity (MGI Ref ID J:13936)
- tremors (MGI Ref ID J:13936)
- head and body tremors
- growth/size phenotype
- decreased body weight (MGI Ref ID J:13936)
- significant reduction in body weight
- cachexia (MGI Ref ID J:13936)
- emaciation by ~P22
- digestive/alimentary phenotype
- abnormal digestive system morphology (MGI Ref ID J:13936)
- beginning at ~P5, stomach contents are reduced
- by ~P22 (time of death), stomach and intestines are devoid of food
- hematopoietic system phenotype
- abnormal spleen morphology (MGI Ref ID J:13936)
- beginning at ~P5, spleen is pale in color
- however, hemoglobin, hematocrit, and mean corpuscular volume (MCV) are within normal range
- small spleen (MGI Ref ID J:13936)
- beginning at ~P5, spleen size is reduced
- homeostasis/metabolism phenotype
- decreased body temperature (MGI Ref ID J:13936)
- hypothermia at ~P22
- liver/biliary system phenotype
- abnormal liver morphology (MGI Ref ID J:13936)
- at P15, livers are devoid of fat and glycogen
- nervous system phenotype
- abnormal brain vasculature (MGI Ref ID J:13936)
- at P15, brains display an abundance of capillaries, suggesting hyperemia
- cardiovascular system phenotype
- abnormal brain vasculature (MGI Ref ID J:13936)
- at P15, brains display an abundance of capillaries, suggesting hyperemia
- immune system phenotype
- abnormal spleen morphology (MGI Ref ID J:13936)
- beginning at ~P5, spleen is pale in color
- however, hemoglobin, hematocrit, and mean corpuscular volume (MCV) are within normal range
- small spleen (MGI Ref ID J:13936)
- beginning at ~P5, spleen size is reduced
This mouse can be used to support research in many areas including:anx related
Metabolism Research
Neurobiology Research
Ataxia (Movement) Defects
Behavioral and Learning Defects
Metabolic Defects
Genes & Alleles
Gene & Allele Information
| Allele Symbol | a | ||
|---|---|---|---|
| Allele Name | nonagouti | ||
| Allele Type | Spontaneous | ||
| Allele Symbol | anx | ||
| Allele Name | anorexia | ||
| Allele Type | Spontaneous | ||
| Strain of Origin | (DW/J x (M. m. domesticus poschiavinus x Swiss))F2 | ||
| Gene Symbol and Name | anx, anorexia | ||
| Chromosome | 2 | ||
| General Note | Phenotypic Similarity to Human Syndrome: Anorexia | ||
Genotyping
Genotyping Information
This strain will not have a genotyping protocol or one is not currently available.
Helpful Links
Genotyping resources and troubleshooting
References
References
Additional References
Broberger C; Johansen J; Johansson C; Schalling M; Hokfelt T. 1998. The neuropeptide Y/agouti gene-related protein (AGRP) brain circuitry in normal, anorectic, and monosodium glutamate-treated mice. Proc Natl Acad Sci U S A 95(25):15043-8. [PubMed: 9844012] [MGI Ref ID J:51566]
Broberger C; Johansen J; Schalling M; Hokfelt T. 1997. Hypothalamic neurohistochemistry of the murine anorexia (anx/anx) mutation: altered processing of neuropeptide Y in the arcuate nucleus. J Comp Neurol 387(1):124-35. [PubMed: 9331176] [MGI Ref ID J:43306]
Jahng JW; Houpt TA; Kim SJ; Joh TH; Son JH. 1998. Neuropeptide Y mRNA and serotonin innervation in the arcuate nucleus of anorexia mutant mice. Brain Res 790(1-2):67-73. [PubMed: 9593828] [MGI Ref ID J:47750]
Maltais LJ; Lane PW; Beamer WG. 1984. Anorexia, a recessive mutation causing starvation in preweanling mice. J Hered 75(6):468-72. [PubMed: 6595305] [MGI Ref ID J:7689]
Son JH; Baker H; Park DH; Joh TH. 1994. Drastic and selective hyperinnervation of central serotonergic neurons in a lethal neurodevelopmental mouse mutant, Anorexia (anx). Brain Res Mol Brain Res 25(1-2):129-34. [PubMed: 7984037] [MGI Ref ID J:19535]
anx relatedBroberger C; Johansen J; Brismar H; Johansson C; Schalling M ; Hokfelt T. 1999. Changes in neuropeptide Y receptors and pro-opiomelanocortin in the anorexia (anx/anx) mouse hypothalamus. J Neurosci 19(16):7130-9. [PubMed: 10436066] [MGI Ref ID J:56665]
Broberger C; Johansen J; Johansson C; Schalling M; Hokfelt T. 1998. The neuropeptide Y/agouti gene-related protein (AGRP) brain circuitry in normal, anorectic, and monosodium glutamate-treated mice. Proc Natl Acad Sci U S A 95(25):15043-8. [PubMed: 9844012] [MGI Ref ID J:51566]
Broberger C; Johansen J; Schalling M; Hokfelt T. 1997. Hypothalamic neurohistochemistry of the murine anorexia (anx/anx) mutation: altered processing of neuropeptide Y in the arcuate nucleus. J Comp Neurol 387(1):124-35. [PubMed: 9331176] [MGI Ref ID J:43306]
Chun HS; Park Y; Yang YK; Kim do K; Son JH; Kim SJ. 2003. Identification of genes showing differential expression in anorexia mutant mouse. Neuroreport 14(7):1055-9. [PubMed: 12802202] [MGI Ref ID J:90062]
Gerke V; Moss SE. 1997. Annexins and membrane dynamics. Biochim Biophys Acta 1357(2):129-54. [PubMed: 9223619] [MGI Ref ID J:41703]
Jahng JW; Houpt TA; Joh TH; Son JH. 1998. Differential expression of monoamine oxidase A, serotonin transporter, tyrosine hydroxylase and norepinephrine transporter mRNA by anorexia mutation and food deprivation. Brain Res Dev Brain Res 107(2):241-6. [PubMed: 9593916] [MGI Ref ID J:109166]
Jahng JW; Houpt TA; Kim SJ; Joh TH; Son JH. 1998. Neuropeptide Y mRNA and serotonin innervation in the arcuate nucleus of anorexia mutant mice. Brain Res 790(1-2):67-73. [PubMed: 9593828] [MGI Ref ID J:47750]
Johansen JE; Broberger C; Lavebratt C; Johansson C; Kuhar MJ; Hokfelt T; Schalling M. 2000. Hypothalamic CART and serum leptin levels are reduced in the anorectic (anx/anx) mouse. Brain Res Mol Brain Res 84(1-2):97-105. [PubMed: 11113536] [MGI Ref ID J:66520]
Johansen JE; Fetissov SO; Bergstrom U; Nilsson I; Fay C; Ranscht B; Hokfelt T; Schalling M. 2007. Evidence for hypothalamic dysregulation in mouse models of anorexia as well as in humans. Physiol Behav 92(1-2):278-82. [PubMed: 17560618] [MGI Ref ID J:136782]
Johansen JE; Teixeira VL; Johansson C; Serrao P; Berggren PO; Soares-Da-Silva P; Schalling M; Bertorello AM. 2001. Altered dopaminergic transmission in the anorexic anx/anx mouse striatum. Neuroreport 12(12):2737-41. [PubMed: 11522958] [MGI Ref ID J:103710]
Kim MJ; Kim Y; Kim SA; Lee HJ; Choe BK; Nam M; Kim BS; Kim JW; Yim SV; Kim CJ; Chung JH. 2001. Increases in cell proliferation and apoptosis in dentate gyrus of anorexia (anx/anx) mice. Neurosci Lett 302(2-3):109-12. [PubMed: 11290399] [MGI Ref ID J:107936]
Lachuer J; Ouyang L; Legras C; Del Rio J; Barlow C. 2005. Gene expression profiling reveals an inflammatory process in the anx/anx mutant mice. Brain Res Mol Brain Res 139(2):372-6. [PubMed: 16006007] [MGI Ref ID J:103396]
Maltais L; Lane PW. 1983. Anorexia (anx) Mouse News Lett 68:72. [MGI Ref ID J:13936]
Maltais LJ; Lane PW; Beamer WG. 1984. Anorexia, a recessive mutation causing starvation in preweanling mice. J Hered 75(6):468-72. [PubMed: 6595305] [MGI Ref ID J:7689]
Mercader JM; Lozano JJ; Sumoy L; Dierssen M; Visa J; Gratacos M; Estivill X. 2008. Hypothalamus transcriptome profile suggests an anorexia-cachexia syndrome in the anx/anx mouse model. Physiol Genomics 35(3):341-50. [PubMed: 18812457] [MGI Ref ID J:145451]
Son JH; Baker H; Park DH; Joh TH. 1994. Drastic and selective hyperinnervation of central serotonergic neurons in a lethal neurodevelopmental mouse mutant, Anorexia (anx). Brain Res Mol Brain Res 25(1-2):129-34. [PubMed: 7984037] [MGI Ref ID J:19535]
Williams CL; Rosenblatt JS; Hall WG. 1979. Inhibition of suckling in weaning-age rats: a possible serotonergic mechanism. J Comp Physiol Psychol 93(3):414-29. [PubMed: 479391] [MGI Ref ID J:28102]
Health & husbandry
Health & Colony Maintenance Information
Currently there no information available for this strain. This may be due to the supply level of this strain.
Purchasing information
Pricing, Supply Level & Notes, Controls, General Terms & Conditions
Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $1900.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Additional Supply Details
| Pricing for International shipping destinations |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $2470.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Additional Supply Details
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Supply Details
| Standard Supply | Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information. |
|---|---|
| Supply Notes |
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Control Information
| Control | ||
|---|---|---|
| Untyped from the colony | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| International - 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 and Purchasing Information
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JAX® Mice, Products & Services Conditions of Use
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