JAX
Mouse Strain Datasheet - 001924
B6EiC3Sn a/A-Ts(1716)65Dn/J
Also Known As: Ts65Dn
Ts65Dn mice are trisomic for about two-thirds of the genes orthologous to human chromosome 21 and are a well-characterized model for studying Down Syndrome.
Read More +Genetic overview
| Genetic Background | Generation |
|---|---|
|
N?+N12
|
Ts(1716)65Dn
| Allele Type | Gene Symbol | Gene Name |
|---|---|---|
| Radiation induced | Ts(1716)65Dn | trisomy, Chr 16 translocation to Chr 17, Davisson 65 |
Base Price
Starting at:
| $247.50 Domestic price for female |
| $425.50 Domestic price for breeder pair |
Important Note
Pde6brd1, the recessive retinal degeneration 1 mutation, is segregating in this colony. Animals that are homozygous for rd1 will be blind. Stock No. 005252 is an alternative strain, with a virtually identical genetic background except that it is wild-type for Pde6brd1.
Detailed Description
Segmentally trisomic Ts(1716)65Dn mice provide a postnatal model for Down syndrome. Ts65Dn mice have three copies of most of the genes on mouse Chr 16 that are homologues of human Chr 21 genes. These extra genes, along with the centromere and about 5% of proximal Chr 17 are contained in a small extra chromosome derived from a reciprocal translocation.
Neural cognitive deficits and behavioral abnormalities have been noted in Ts65Dn mice. They have spatial learning and memory defects as assessed in the Morris water maze and the radial arm maze, show developmental delay in sensorimotor milestones, and exhibit locomotor hyperactivity, lack of behavioral inhibition, and stereotypic behavior. They perform similar to controls in visual placing, balance, prehensile reflex and traction on a horizontal bar, motor coordination, swimming ability and olfaction orienting. They also show altered noradrenergic transmission in the hippocampus and cerebral cortex and degeneration of basal forebrain cholinergic neurons by 6 months of age. Trisomic females are smaller and produce fewer, smaller litters than euploid females while trisomic males are effectively sterile with hypospermia.
The precise locations of the Chr 16 and Chr 17 breakpoints are 84,351,351 bp and 9,426,822 bp, respectively. The Chr 16 segment contains about two thirds of the human Chr 21 homologues in the mouse, from mitochondrial ribosomal protein L39 (Mrpl39) gene to the distal telomere. These data were used to generate a PCR genotyping assay for Ts65Dn (Reinholdt et al., 2011), replacing the previous methods of chromosome analysis or qPCR. For comparison of segments conserved in human Chr 21 with mouse Chrs 16, 17, 10 and genetic definition of Ts65Dn, see the Human - Mouse Orthology Map. Northern and Western blotting, enzyme activity assays and reverse phase protein arrays (RPPA) demonstrate that some but not all genes in the translocation product are expressed at elevated levels in segmentally trisomic animals. RPPA shows a loss of correlation among some brain proteins (Ahmed et al., 2012).
Please see the Down Syndrome and Cytogenetics Models Resource for more information.
Development
Cesium irradiation was used to produce a reciprocal translocation, T (16;17) 65Dn. One of the translocation chromosomes is a small marker chromosome, comprised of the centromere and proximal end of Chr 17 (~9.5Mb) and the distal end of mouse Chr 16 (~34Mb). Translocation heterozygous females produced progeny trisomic for this small translocation product and a stock was established in which Ts65Dn mice are trisomic for the genes carried in the small translocation chromosome, symbolized Ts(1716)65Dn.
Control Suggestions
Selected References
- Ahmed MM; Sturgeon X; Ellison M; Davisson MT; Gardiner KJ. 2012. Loss of Correlations among Proteins in Brains of the Ts65Dn Mouse Model of Down Syndrome. J Proteome Res 11(2):1251-63. PubMed: 22214338MGI: J:180732
- Reeves RH; Irving NG; Moran TH; Wohn A; Kitt C; Sisodia SS; Schmidt C; Bronson RT; Davisson MT. 1995. A mouse model for Down syndrome exhibits learning and behaviour deficits [see comments] Nat Genet 11(2):177-84. PubMed: 7550346MGI: J:29232
- Reinholdt LG; Ding Y; Gilbert GT; Czechanski A; Solzak JP; Roper RJ; Johnson MT; Donahue LR; Lutz C; Davisson MT. 2011. Molecular characterization of the translocation breakpoints in the Down syndrome mouse model Ts65Dn. Mamm Genome 22(11-12):685-91. PubMed: 21953412MGI: J:178871
Ts(1716)65Dn
Allele Symbol: Ts(1716)65Dn
| Allele Name | trisomy, Chr 16 translocation to Chr 17, Davisson 65 |
|---|---|
| Allele Type | Radiation induced |
| Allele Synonym(s) | T(16C3-4;17A2)65Dn; Ts16; Ts65Dn |
| Gene Symbol and Name | Ts(1716)65Dn, trisomy, Chr 16 translocation to Chr 17, Davisson 65 |
| Gene Synonym(s) | Ts65Dn; trisomy 16 |
| Strain of Origin | DBA/2J |
| Chromosome | 16 |
| Molecular Note | About 15% of the distal end of chromosome 16 is fused to less than 10% of the centromeric end of chromosome 17 to form a small translocation chromosome. The translocation breaks mouse Chr 16 just proximal to the amyloid precursor protein ( App ) gene and contains the HSA21-homologous genes from App to the telomere. The translocation chromosome also contains the centromere and a small portion (~5%) of Chr 17. Northern and Western blotting and enzyme activity assays demonstrate that genes on the translocation product are expressed at elevated levels in segmentally trisomic animals. |
Disease Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
- Neurobiology Research
- Down syndrome
Mammalian Phenotype Terms by Genotype
Genotype: Ts(1716)65Dn/0
B6EiC3Sn.BLiA-Ts(1716)65Dn/DnJ
growth/size/body region phenotype
- decreased body length
- the length from the nost to the tip of the tail is shorter than in background controls, although the length from the nose to the base of the tail does not have a statistically significant difference (MGI Ref ID J:153579)
- decreased body weight
- (MGI Ref ID J:153579)
behavior/neurological phenotype
- abnormal learning/memory/conditioning
- in 22 degree water there is increased latency of acquisition of the hidden platform in the Morris water maze test (MGI Ref ID J:153579)
- abnormal spatial learning
- (MGI Ref ID J:153579)
- decreased grip strength
- output of a grip strength meter shows reduced grip force relative to controls (MGI Ref ID J:153579)
- hyperactivity
- although activity during the light cycle is not different from that of controls, during the dark cycle the total activity is significantly greater than in background controls (MGI Ref ID J:153579)
- impaired contextual conditioning behavior
- (MGI Ref ID J:153579)
- impaired cued conditioning behavior
- (MGI Ref ID J:153579)
- increased stereotypic behavior
- significantly increased dark cycle horizontal and vertical stereotypic activity (MGI Ref ID J:153579)
- increased vertical activity
- significantly increased dark cycle rearing (MGI Ref ID J:153579)
The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain
Genotype: Ts(1716)65Dn/0
involves: C3H/HeJ * C57BL/6JEi * DBA/2J
nervous system phenotype
- abnormal Purkinje cell morphology
- Purkinje cell linear density is decreased compared to in wild-type mice (MGI Ref ID J:91221)
Genotype: Ts(1716)65Dn/0
involves: C3H/HeSnJ * C57BL/6JEi * DBA/2J
reproductive system phenotype
- abnormal Sertoli cell morphology
- only a few Sertoli cells are visible; germ cells appear to be detached from the remaining Sertoli cells (MGI Ref ID J:96650)
- abnormal male germ cell morphology
- significantly more sperm with head abnormalities (MGI Ref ID J:117029)
- abnormal spermatogenesis
- abnormal testis morphology
- Leydig cells are clustered loosely in expanded interstitial compartment (MGI Ref ID J:96650)
- arrest of male meiosis
- many tubules contain germ cells in arrested at meiotic metaphase 1 (MGI Ref ID J:117029)
- decreased sperm progressive motility
- significantly reduced frequencies of sperm with progressive motility (MGI Ref ID J:117029)
- decreased testis weight
- male infertility
- oligozoospermia
- sperm concentration was significantly reduced below controls (MGI Ref ID J:117029)
cellular phenotype
- abnormal male germ cell morphology
- significantly more sperm with head abnormalities (MGI Ref ID J:117029)
- oligozoospermia
- sperm concentration was significantly reduced below controls (MGI Ref ID J:117029)
growth/size/body region phenotype
- decreased body size
- mice are ~20% smaller in size compared to normal littermates postnatally (MGI Ref ID J:96650)
- decreased body weight
- (MGI Ref ID J:94569)
nervous system phenotype
- abnormal CNS synapse formation
- 18% of dendritic spines are enlarged and display irregular heads or a globular shape (MGI Ref ID J:94569)
- average synapse length is increased 34% in the hippocampus and 25% in the cortex (MGI Ref ID J:94569)
- glutamatergic synapses are distributed 33% on the dendritic shaft (compared to 51% in wild-type mice) and 67% (compared to 49% in wild-type mice) on the heads or necks of the dendritic spines (MGI Ref ID J:94569)
- in young and old mice alike, small presynaptic boutons are decreased and large presynaptic boutons are increased in the fascia dentate and motor cortex with the average diameter of a presynaptic bouton increased by 40% in the cortex (MGI Ref ID J:94569)
- the area of presynaptic elements (p38+) is increased in the fascia dentate and motor cortex (MGI Ref ID J:94569)
- abnormal cerebellar granule cell morphology
- dendritic spine density on granule cells is decreased on average by 17% compared to in wild-type mice (MGI Ref ID J:94569)
- abnormal dendrite morphology
- abnormal neuron morphology
- in fascia dentate, spine density is significantly decreased on dendrites of granule cells; dendritic spines are significantly enlarged; dendritic width is similar to controls (MGI Ref ID J:96650)
endocrine/exocrine gland phenotype
- abnormal Sertoli cell morphology
- only a few Sertoli cells are visible; germ cells appear to be detached from the remaining Sertoli cells (MGI Ref ID J:96650)
- abnormal testis morphology
- Leydig cells are clustered loosely in expanded interstitial compartment (MGI Ref ID J:96650)
Genotype: Ts(1716)65Dn/0
involves: C3H/HeJ * C57BL/6 * DBA/2J
nervous system phenotype
- abnormal cerebellar granule cell morphology
- granule cell density is reduced to 76% of that in control mice (MGI Ref ID J:121764)
- decreased Purkinje cell number
- Purkinje cell density is reduced to 90% of that in control mice (MGI Ref ID J:121764)
- increased brain size
- (MGI Ref ID J:121764)
- small cerebellum
- cerebellar volume is reduced to 88% of that in control mice (MGI Ref ID J:121764)
behavior/neurological phenotype
- abnormal spatial learning
- mice show impairment in a Morris water maze test (MGI Ref ID J:121764)
growth/size/body region phenotype
- decreased body weight
- (MGI Ref ID J:121764)
Genotype: Ts(1716)65Dn/0
involves: C3H * C57BL/6 * DBA/2J
craniofacial phenotype
- abnormal incisor morphology
- mice exhibit a reduction in the height of the incisive alveolar segment compared to in wild-type mice (MGI Ref ID J:73800)
- abnormal mandibular angle morphology
- reduced in size compared to in wild-type mice (MGI Ref ID J:73800)
- abnormal mandibular coronoid process morphology
- reduced in size compared to in wild-type mice (MGI Ref ID J:73800)
- decreased cranium height
- mice exhibit a more generalized shortening of the skull along the anterior posterior axis compared to in Ts(1216)1Cje mice (MGI Ref ID J:73800)
- small mandible
- (MGI Ref ID J:73800)
skeleton phenotype
- abnormal incisor morphology
- mice exhibit a reduction in the height of the incisive alveolar segment compared to in wild-type mice (MGI Ref ID J:73800)
- abnormal mandibular angle morphology
- reduced in size compared to in wild-type mice (MGI Ref ID J:73800)
- abnormal mandibular coronoid process morphology
- reduced in size compared to in wild-type mice (MGI Ref ID J:73800)
- decreased cranium height
- mice exhibit a more generalized shortening of the skull along the anterior posterior axis compared to in Ts(1216)1Cje mice (MGI Ref ID J:73800)
- small mandible
- (MGI Ref ID J:73800)
growth/size/body region phenotype
- abnormal incisor morphology
- mice exhibit a reduction in the height of the incisive alveolar segment compared to in wild-type mice (MGI Ref ID J:73800)
Genotype: Ts(1716)65Dn/0
involves: DBA/2J
craniofacial phenotype
- abnormal neurocranium morphology
- cranial vault is enlarged (MGI Ref ID J:93223)
- small cranium
- size difference was most pronounced along the rostralcaudal axis (MGI Ref ID J:93223)
- small mandible
- mice show a Down's Syndrome-like pattern of mandible reduction (MGI Ref ID J:93223)
limbs/digits/tail phenotype
- short femur
- (MGI Ref ID J:93223)
skeleton phenotype
- abnormal neurocranium morphology
- cranial vault is enlarged (MGI Ref ID J:93223)
- short femur
- (MGI Ref ID J:93223)
- small cranium
- size difference was most pronounced along the rostralcaudal axis (MGI Ref ID J:93223)
- small mandible
- mice show a Down's Syndrome-like pattern of mandible reduction (MGI Ref ID J:93223)
Genotype: Ts(1716)65Dn/0
involves: C3H/HeJ * C57BL/6J * DBA/2J
neoplasm
- increased follicular lymphoma incidence
- splenic architecture is replaced by proliferated immature mononuclear cells arranged in follicular aggregates indicating follicular lymphoma (MGI Ref ID J:174270)
- increased lymphoma incidence
- increased malignant tumor incidence
- some mutants exhibit malignant tumors of liver, colon, or lung (MGI Ref ID J:174270)
immune system phenotype
- abnormal spleen B cell follicle morphology
- splenic white pulp contains follicles that are larger and more irregular in shape than normal follicles and are often fused with adjacent follicles (MGI Ref ID J:174270)
- abnormal spleen red pulp morphology
- splenic red pulp is largely obliterated (MGI Ref ID J:174270)
hematopoietic system phenotype
- abnormal spleen B cell follicle morphology
- splenic white pulp contains follicles that are larger and more irregular in shape than normal follicles and are often fused with adjacent follicles (MGI Ref ID J:174270)
- abnormal spleen red pulp morphology
- splenic red pulp is largely obliterated (MGI Ref ID J:174270)
Genotype: Ts(1716)65Dn/0
involves: C3H/HeH * C3H/HeSn * C57BL/6Ei * C57BL/6J * DBA/2J
mortality/aging
- postnatal lethality, incomplete penetrance
- (MGI Ref ID J:185269)
cardiovascular system phenotype
- abnormal QRS complex
- fragmented time-course with decreased S wave amplitude (MGI Ref ID J:185269)
- abnormal heart electrocardiography waveform feature
- flecainide-treated mice exhibit a specific electrophysiologic signature as compare to wild-type mice (MGI Ref ID J:185269)
- abnormal heart morphology
- great vessel and cardiac malformation in 1 of 18 mice that died postnatally (MGI Ref ID J:185269)
- decreased P wave amplitude
- in the frontal plane (MGI Ref ID J:185269)
- decreased QRS amplitude
- (MGI Ref ID J:185269)
- decreased heart rate
- (MGI Ref ID J:185269)
- prolonged PR interval
- (MGI Ref ID J:185269)
- prolonged QRS complex duration
- (MGI Ref ID J:185269)
- prolonged QT interval
- larger QT and QTc (MGI Ref ID J:185269)
- prolonged RR interval
- (MGI Ref ID J:185269)
- retroesophageal right subclavian artery
- aberrant right subclavian artery arising from the distal part of the aortic arch (MGI Ref ID J:185269)
- ventricular septal defect
- 1 in 18 newborns exhibit an upper communication of the ventricles, indication a septation defect of the ventricles (MGI Ref ID J:185269)
References
- Ahmed MM; Sturgeon X; Ellison M; Davisson MT; Gardiner KJ. 2012. Loss of Correlations among Proteins in Brains of the Ts65Dn Mouse Model of Down Syndrome. J Proteome Res 11(2):1251-63. PubMed: 22214338MGI: J:180732
- Reeves RH; Irving NG; Moran TH; Wohn A; Kitt C; Sisodia SS; Schmidt C; Bronson RT; Davisson MT. 1995. A mouse model for Down syndrome exhibits learning and behaviour deficits [see comments] Nat Genet 11(2):177-84. PubMed: 7550346MGI: J:29232
- Reinholdt LG; Ding Y; Gilbert GT; Czechanski A; Solzak JP; Roper RJ; Johnson MT; Donahue LR; Lutz C; Davisson MT. 2011. Molecular characterization of the translocation breakpoints in the Down syndrome mouse model Ts65Dn. Mamm Genome 22(11-12):685-91. PubMed: 21953412MGI: J:178871
Additional References
- Belichenko NP; Belichenko PV; Kleschevnikov AM; Salehi A; Reeves RH; Mobley WC. 2009. The 'Down syndrome critical region' is sufficient in the mouse model to confer behavioral, neurophysiological, and synaptic phenotypes characteristic of Down syndrome. J Neurosci 29(18):5938-48. PubMed: 19420260MGI: J:148478
- Davisson M; Akeson E; Schmidt C; Harris B; Farley J; Handel MA. 2007. Impact of trisomy on fertility and meiosis in male mice. Hum Reprod 22(2):468-76. PubMed: 17050550MGI: J:117029
- Davisson MT; Bechtel LJ; Akeson EC; Fortna A; Slavov D; Gardiner K. 2001. Evolutionary breakpoints on human chromosome 21. Genomics 78(1/2):99-106. PubMed: 11707078MGI: J:69673
- Dierssen M; Vallina IF; Baamonde C; Garcia-Calatayud S; Lumbreras MA; Florez J. 1997. Alterations of central noradrenergic transmission in Ts65Dn mouse, a model for Down syndrome. Brain Res 749(2):238-44. PubMed: 9138724MGI: J:39408
- Hill JM; Ades AM; McCune SK; Sahir N; Moody EM; Abebe DT; Crnic LS; Brenneman DE. 2003. Vasoactive intestinal peptide in the brain of a mouse model for Down syndrome. Exp Neurol 183(1):56-65. PubMed: 12957488MGI: J:85337
- Holtzman DM; Santucci D; Kilbridge J; Chua-Couzens J; Fontana DJ; Daniels SE; Johnson RM; Chen K; Sun Y; Carlson E; Alleva E; Epstein CJ; Mobley WC. 1996. Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome. Proc Natl Acad Sci U S A 93(23):13333-8. PubMed: 8917591MGI: J:36555
- Liu DP; Schmidt C; Billings T; Davisson MT. 2003. Quantitative PCR genotyping assay for the Ts65Dn mouse model of Down syndrome. Biotechniques 35(6):1170-4, 1176, 1178 passim. PubMed: 14682051MGI: J:112549
Additional - Ts(1716)65Dn related
- Adorno M; Sikandar S; Mitra SS; Kuo A; Nicolis Di Robilant B; Haro-Acosta V; Ouadah Y; Quarta M; Rodriguez J; Qian D; Reddy VM; Cheshier S; Garner CC; Clarke MF. 2013. Usp16 contributes to somatic stem-cell defects in Down's syndrome. Nature 501(7467):380-4. PubMed: 24025767MGI: J:206099
- Akeson EC; Lambert JP; Narayanswami S; Gardiner K; Bechtel LJ; Davisson MT. 2001. Ts65Dn -- localization of the translocation breakpoint and trisomic gene content in a mouse model for Down syndrome. Cytogenet Cell Genet 93(3-4):270-6. PubMed: 11528125MGI: J:71031
- Alldred MJ; Lee SH; Petkova E; Ginsberg SD. 2015. Expression profile analysis of vulnerable CA1 pyramidal neurons in young-Middle-Aged Ts65Dn mice. J Comp Neurol 523(1):61-74. PubMed: 25131634MGI: J:238190
- Altafaj X; Martin ED; Ortiz-Abalia J; Valderrama A; Lao-Peregrin C; Dierssen M; Fillat C. 2013. Normalization of Dyrk1A expression by AAV2/1-shDyrk1A attenuates hippocampal-dependent defects in the Ts65Dn mouse model of Down syndrome. Neurobiol Dis 52:117-27. PubMed: 23220201MGI: J:197665
- Arriagada C; Bustamante M; Atwater I; Rojas E; Caviedes R; Caviedes P. 2010. Apoptosis is directly related to intracellular amyloid accumulation in a cell line derived from the cerebral cortex of a trisomy 16 mouse, an animal model of Down syndrome. Neurosci Lett 470(1):81-5. PubMed: 20043975MGI: J:156873
- Ash JA; Velazquez R; Kelley CM; Powers BE; Ginsberg SD; Mufson EJ; Strupp BJ. 2014. Maternal choline supplementation improves spatial mapping and increases basal forebrain cholinergic neuron number and size in aged Ts65Dn mice. Neurobiol Dis 70:32-42. PubMed: 24932939MGI: J:218355
- Aso S; Miyabara S; Sugihara H; Winking H. 2001. Comparative study of mouse trisomy 16 and bis-diamine treated fetuses: Discrimination of possible contribution of neural crest cells to malformations Cong Anom 41:169-176. MGI: J:104833
- Ayberk Kurt M; Ilker Kafa M; Dierssen M; Ceri Davies D. 2004. Deficits of neuronal density in CA1 and synaptic density in the dentate gyrus, CA3 and CA1, in a mouse model of Down syndrome. Brain Res 1022(1-2):101-9. PubMed: 15353219MGI: J:92543
- Baek KH; Zaslavsky A; Lynch RC; Britt C; Okada Y; Siarey RJ; Lensch MW; Park IH; Yoon SS; Minami T; Korenberg JR; Folkman J; Daley GQ; Aird WC; Galdzicki Z; Ryeom S. 2009. Down's syndrome suppression of tumour growth and the role of the calcineurin inhibitor DSCR1. Nature 459(7250):1126-30. PubMed: 19458618MGI: J:150286
- Bambrick LL; Yarowsky PJ; Krueger BK. 2003. Altered astrocyte calcium homeostasis and proliferation in theTs65Dn mouse, a model of Down syndrome. J Neurosci Res 73(1):89-94. PubMed: 12815712MGI: J:173986
- Baxter LL; Moran TH; Richtsmeier JT; Troncoso J; Reeves RH. 2000. Discovery and genetic localization of Down syndrome cerebellar phenotypes using the Ts65Dn mouse. Hum Mol Genet 9(2):195-202. PubMed: 10607830MGI: J:59886
- Bearer EL; Zhang X; Jacobs RE. 2007. Live imaging of neuronal connections by magnetic resonance: Robust transport in the hippocampal-septal memory circuit in a mouse model of Down syndrome. Neuroimage 37(1):230-42. PubMed: 17566763MGI: J:173981
- Begenisic T; Sansevero G; Baroncelli L; Cioni G; Sale A. 2015. Early environmental therapy rescues brain development in a mouse model of Down syndrome. Neurobiol Dis 82:409-19. PubMed: 26244989MGI: J:227677
- Begenisic T; Spolidoro M; Braschi C; Baroncelli L; Milanese M; Pietra G; Fabbri ME; Bonanno G; Cioni G; Maffei L; Sale A. 2011. Environmental enrichment decreases GABAergic inhibition and improves cognitive abilities, synaptic plasticity, and visual functions in a mouse model of Down syndrome. Front Cell Neurosci 5:29. PubMed: 22207837MGI: J:190265
- Belichenko PV; Kleschevnikov AM; Masliah E; Wu C; Takimoto-Kimura R; Salehi A; Mobley WC. 2009. Excitatory-inhibitory relationship in the fascia dentata in the Ts65Dn mouse model of Down syndrome. J Comp Neurol 512(4):453-66. PubMed: 19034952MGI: J:173987
- Belichenko PV; Kleschevnikov AM; Salehi A; Epstein CJ; Mobley WC. 2007. Synaptic and cognitive abnormalities in mouse models of Down syndrome: exploring genotype-phenotype relationships. J Comp Neurol 504(4):329-45. PubMed: 17663443MGI: J:132525
- Belichenko PV; Masliah E; Kleschevnikov AM; Villar AJ; Epstein CJ; Salehi A; Mobley WC. 2004. Synaptic structural abnormalities in the Ts65Dn mouse model of Down Syndrome. J Comp Neurol 480(3):281-98. PubMed: 15515178MGI: J:94569
- Berg BM; Croom J; Fernandez JM; Spears JW; Eisen EJ; Taylor IL; Daniel LR; Coles BA; Boeheim F; Mannon PJ. 2000. Peptide YY administration decreases brain aluminum in the Ts65Dn Down syndrome mouse model Growth Dev Aging 64(1-2):3-19. PubMed: 10969882MGI: J:63856
- Berndt A; Sundberg BA; Silva KA; Kennedy VE; Richardson MA; Li Q; Bronson RT; Uitto J; Sundberg JP. 2014. Phenotypic characterization of the KK/HlJ inbred mouse strain. Vet Pathol 51(4):846-57. PubMed: 24009271MGI: J:227536
- Best TK; Cho-Clark M; Siarey RJ; Galdzicki Z. 2008. Speeding of miniature excitatory post-synaptic currents in Ts65Dn cultured hippocampal neurons. Neurosci Lett 438(3):356-61. PubMed: 18490108MGI: J:173980
- Best TK; Cramer NP; Chakrabarti L; Haydar TF; Galdzicki Z. 2012. Dysfunctional hippocampal inhibition in the Ts65Dn mouse model of Down syndrome. Exp Neurol 233(2):749-57. PubMed: 22178330MGI: J:182047
- Best TK; Siarey RJ; Galdzicki Z. 2007. Ts65Dn, a mouse model of Down syndrome, exhibits increased GABAB-induced potassium current. J Neurophysiol 97(1):892-900. PubMed: 17093127MGI: J:135917
- Bhutta MF; Cheeseman MT; Herault Y; Yu YE; Brown SD. 2013. Surveying the Down syndrome mouse model resource identifies critical regions responsible for chronic otitis media. Mamm Genome :. PubMed: 24068166MGI: J:201811
- Bianchi P; Bettini S; Guidi S; Ciani E; Trazzi S; Stagni F; Ragazzi E; Franceschini V; Bartesaghi R. 2014. Age-related impairment of olfactory bulb neurogenesis in the Ts65Dn mouse model of Down syndrome. Exp Neurol 251:1-11. PubMed: 24192151MGI: J:206601
- Bianchi P; Ciani E; Contestabile A; Guidi S; Bartesaghi R. 2010. Lithium restores neurogenesis in the subventricular zone of the Ts65Dn mouse, a model for Down syndrome. Brain Pathol 20(1):106-18. PubMed: 19298631MGI: J:173984
- Bimonte-Nelson HA; Hunter CL; Nelson ME; Granholm AC. 2003. Frontal cortex BDNF levels correlate with working memory in an animal model of Down syndrome. Behav Brain Res 139(1-2):47-57. PubMed: 12642175MGI: J:95711
- Blank M; Fuerst PG; Stevens B; Nouri N; Kirkby L; Warrier D; Barres BA; Feller MB; Huberman AD; Burgess RW; Garner CC. 2011. The Down Syndrome Critical Region Regulates Retinogeniculate Refinement. J Neurosci 31(15):5764-5776. PubMed: 21490218MGI: J:170968
- Blazek JD; Abeysekera I; Li J; Roper RJ. 2015. Rescue of the abnormal skeletal phenotype in Ts65Dn Down syndrome mice using genetic and therapeutic modulation of trisomic Dyrk1a. Hum Mol Genet 24(20):5687-96. PubMed: 26206885MGI: J:226041
- Blazek JD; Billingsley CN; Newbauer A; Roper RJ. 2010. Embryonic and not maternal trisomy causes developmental attenuation in the Ts65Dn mouse model for Down syndrome. Dev Dyn 239(6):1645-53. PubMed: 20503361MGI: J:160592
- Blazek JD; Gaddy A; Meyer R; Roper RJ; Li J. 2011. Disruption of bone development and homeostasis by trisomy in Ts65Dn Down syndrome mice. Bone 48(2):275-80. PubMed: 20870049MGI: J:170199
- Blazek JD; Malik AM; Tischbein M; Arbones ML; Moore CS; Roper RJ. 2014. Abnormal mineralization of the Ts65Dn Down syndrome mouse appendicular skeleton begins during embryonic development in a Dyrk1a-independent manner. Mech Dev :. PubMed: 25556111MGI: J:217672
- Casas C; Martinez S; Pritchard MA; Fuentes JJ; Nadal M; Guimera J; Arbones M; Florez J; Soriano E; Estivill X; Alcantara S. 2001. Dscr1, a novel endogenous inhibitor of calcineurin signaling, is expressed in the primitive ventricle of the heart and during neurogenesis. Mech Dev 101(1-2):289-92. PubMed: 11231093MGI: J:68156
- Cataldo AM; Petanceska S; Peterhoff CM; Terio NB; Epstein CJ; Villar A; Carlson EJ; Staufenbiel M; Nixon RA. 2003. App gene dosage modulates endosomal abnormalities of Alzheimer's disease in a segmental trisomy 16 mouse model of down syndrome. J Neurosci 23(17):6788-92. PubMed: 12890772MGI: J:84685
- Cefalu JA; Croom WJ Jr; Eisen EJ; Jones EE; Daniel LR; Taylor IL. 1998. Jejunal function and plasma amino acid concentrations in the segmental trisomic Ts65Dn mouse. Growth Dev Aging 62(1-2):47-59. PubMed: 9666356MGI: J:48496
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