A behavioral assessment of Ts65Dn mice: a putative Down syndrome model

Escorihuela, Rosa M.; Fernández-Teruel, Alberto; Vallina, Iria F.; Baamonde, Carmela; Lumbreras, M; Dierssen, Mara; Tobeña, Adolf; Flórez, Jesús

doi:10.1016/0304-3940(95)12052-6

Cited by 240 publications

(197 citation statements)

References 10 publications

Supporting

Mentioning

163

Contrasting

Unclassified

Order By: Relevance

“…On a test of working and reference memory in a water-escape radialarm maze task, learning was impaired in both 4-and 6-month-old Ts65Dn mice . In most other studies, learning and memory deficits in Ts65Dn mice were found at 6 months or older (Demas et al, 1996;Escorihuela et al, 1995Escorihuela et al, , 1998Holtzman et al, 1996;Reeves et al, 1995), although deficits in Ts65Dn mice on some versions of swim tasks are evident as early as 4 months of age (Seo and Isacson, 2005). Thus, the present findings are generally consistent with many reports of memory impairments in this partial trisomy model of Down syndrome, most examining mice at 6 months and older (cf.…”

Section: Spontaneous Alternationsupporting

confidence: 91%

See 1 more Smart Citation

Age-related changes in memory and in acetylcholine functions in the hippocampus in the Ts65Dn mouse, a model of Down syndrome

Chang

Gold

2008

Neurobiology of Learning and Memory

View full text Add to dashboard Cite

Spatial working memory and the ability of a cholinesterase inhibitor to enhance memory were assessed at 4, 10, and 16 months of ages in control and Ts65Dn mice, a partial trisomy model of Down syndrome, with possibly significant relationships to Alzheimer's Disease as well. In addition, ACh release during memory testing was measured in samples collected from the hippocampus using in vivo microdialysis at 4, 10, and 22-25 months of age. When tested on a four-arm spontaneous alternation task, the Ts65Dn mice exhibited impaired memory scores at both 4 and 10 months. At 16 months, control performance had declined toward that of the Ts65Dn mice and the difference in scores across genotypes was not significant. Physostigmine (50 μg/kg) fully reversed memory deficits in the Ts65Dn mice in the 4-month-old group but not in older mice. Ts65Dn and control mice exhibited comparable baseline levels of ACh release at all ages tested; these levels did not decline significantly across age in either genotype. ACh release increased significantly during alternation testing only in the young Ts65Dn and control mice. However, the increase in ACh release during alternation testing was significantly greater in control than Ts65Dn mice at this age. The controls exhibited a significant age-related decline in the testing-related increase in ACh release. With only a small increase during testing in young Ts65Dn mice, the age-related decline in responsiveness of ACh release to testing was not significant in these mice. Overall, these results suggest that diminished responsiveness of ACh release in the hippocampus to behavioral testing may contribute memory impairments in Ts65Dn mice.

show abstract

Section: Spontaneous Alternationsupporting

confidence: 91%

“…However, learning and memory are not impaired in all tasks. Cued learning in the swim task is preserved in the Ts65Dn mice (Escorihuela et al, 1995;Sago et al, 2000), as is memory needed to discriminate very dissimilar contexts (Hyde and Crnic, 2001) and memory for inhibitory avoidance training (Coussons-Read and Crnic, 1996).…”

Section: Introductionmentioning

confidence: 99%

Age-related changes in memory and in acetylcholine functions in the hippocampus in the Ts65Dn mouse, a model of Down syndrome

Chang

Gold

2008

Neurobiology of Learning and Memory

View full text Add to dashboard Cite

show abstract

“…Ts65Dn mice also show a reduction in cerebellum size, as well as the number of cerebral granule cells (Baxter, Moran, Richtsmeier, Troncoso, & Reeves, 2000). Ts65Dn mice have significant deficits in tasks that depend on the functional integrity of the hippocampal formation and associated neocortical circuits, including the Morris water maze spatial learning task and novel object recognition (Escorihuela et al, 1995;L. A. Hyde, Frisone, & Crnic, 2001;Reeves et al, 1995;Sago et al, 2000).…”

Section: Individuals With Ds Display Developmental Alterations In Bramentioning

confidence: 99%

Low dose EGCG treatment beginning in adolescence does not improve cognitive impairment in a Down syndrome mouse model

Stringer

Abeysekera

Dria

et al. 2015

Pharmacology Biochemistry and Behavior

View full text Add to dashboard Cite

“…This segment contains approximately 140 genes, many of which are highly conserved between mice and humans (Gardiner et al 2003). These mice display delays in the acquisition of a number of sensory and motor tasks (Holtzman et al 1996;Costa et al 1999), as well as defects in learning and in the execution of memory tasks mediated by the hippocampus (Reeves et al 1995;Escorihuela et al 1995Escorihuela et al , 1998Holtzman et al 1996).…”

Section: Introductionmentioning

confidence: 99%

Alteration of inhibitory circuits in the somatosensory cortex of Ts65Dn mice, a model for Down’s syndrome

et al. 2010

View full text Add to dashboard Cite

Down's syndrome (DS), with an incidence of one in 800 live births, is the most common genetic disorder associated with mental retardation. This trisomy on chromosome 21 induces a variable phenotype in which the only common feature is the presence of mental retardation. The neural mechanisms underlying mental retardation might include defects in the formation of neuronal networks and neural plasticity. DS patients have alterations in the morphology, the density and the distribution of dendritic spines in the pyramidal neurons of the cortex. Our hypothesis is that the deficits in dendritic arborization observed in the principal neurons of DS patients and Ts65Dn mice (a model for DS that mimics most of the structural alterations observed in humans) may be mediated to some extent by changes in their inhibitory inputs. Different types of interneurons control different types of inhibition. Therefore, to understand well the changes in inhibition in DS, it is necessary to study the different types of interneurons separately. We have studied the expression of synaptophysin, Glutamic acid decarboxylase-67 (GAD-67) and calcium-binding protein-expressing cells in the primary somatosensory cortex of 4-5 month old Ts65Dn mice. We have observed an increment of GAD67 immunoreactivity that is related mainly to an increment of calretinin-immunoreactive cells and among them the ones with bipolar morphology. Since there is a propensity for epilepsy in DS patients, this increase in interneurons might reflect an attempt by the system to block overexcitation rather than an increment in total inhibition and could explain the deficit in interneurons and principal cells observed in elderly DS patients.

show abstract

A behavioral assessment of Ts65Dn mice: a putative Down syndrome model

Cited by 240 publications

References 10 publications

Age-related changes in memory and in acetylcholine functions in the hippocampus in the Ts65Dn mouse, a model of Down syndrome

Age-related changes in memory and in acetylcholine functions in the hippocampus in the Ts65Dn mouse, a model of Down syndrome

Low dose EGCG treatment beginning in adolescence does not improve cognitive impairment in a Down syndrome mouse model

Alteration of inhibitory circuits in the somatosensory cortex of Ts65Dn mice, a model for Down’s syndrome

Contact Info

Product

Resources

About