Frontal cortex BDNF levels correlate with working memory in an animal model of Down syndrome

Bimonte‐Nelson, Heather A.; Hunter, Christopher L.; Nelson, Matthew; Granholm, Ann Charlotte

doi:10.1016/s0166-4328(02)00082-7

Cited by 137 publications

(116 citation statements)

References 52 publications

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“…Therefore, it is likely, and the initial difference in performance of TgCRND8 mice during the first day of training could be caused by subtle differences in their reactivity to altered conditions after the curtain present during nonspatial pretraining was removed. A similar, transient initial difference in escape latencies to a cued platform was observed in the Tg65Dn mouse model of Down syndrome (Bimonte-Nelson et al 2003). In a conventional reference memory test, all mice improved their performance over training (F (3, 24) = 4.5, p < 0.05, days factor), but TgCRND8 mice showed significantly longer escape latency than non-Tg littermates (F (1,8) = 27.2, p < 0.01, genotype factor; Fig.…”

Section: Reference Memory In Tgcrnd8 Micesupporting

confidence: 65%

Search Strategies Used byAPPTransgenic Mice During Navigation in the Morris Water Maze

Janus¹

2004

Learn. Mem.

188

157

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TgCRND8 mice represent a transgenic mouse model of Alzheimer's disease, with onset of cognitive impairment and increasing amyloid-␤ plaques in their brains at 12 weeks of age. In this study, the spatial memory in 25-to 30-week-old TgCRND8 mice was analyzed in two reference and one working memory Morris water maze (MWM) tests. In reference memory tests, the mice were trained to escape to a hidden platform, which in one version of the test was marked by a visual cue. In the working memory test, the hidden platform was moved daily to different locations. The TgCRND8 mice were impaired in reference memory when trained in a hidden platform test. However, the mice developed spatial memory comparable to non-Tg littermates in a cued reference memory test. The mice showed also an impairment in spatial working memory. Analysis of search paths revealed that in contrast to non-Tg littermates, TgCRND8 mice did not use spatial strategies during their navigation. Instead, they learned to locate an escape platform using a nonspatial, chaining strategy. The study showed that (1) the impairment in the reference memory of TgCRND8 mice was reduced when a hidden platform was cued, and that (2) both working and reference memory systems of TgCRND8 mice, but not (3) the plasticity of choice between search strategies, are compromised by the transgene-induced pathology.

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Section: Reference Memory In Tgcrnd8 Micesupporting

confidence: 65%

Search Strategies Used byAPPTransgenic Mice During Navigation in the Morris Water Maze

Janus¹

2004

Learn. Mem.

188

157

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“…However, it is certainly the case that alterations in other brain areas are important to the neural and cognitive impairments in these mice. In this regard, changes in brain-derived neurotrophic functions are evident in frontal cortex (Bimonte-Nelson et al, 2003) as well as hippocampus. Also, as in humans with Down syndrome (cf.…”

Section: General Conclusionmentioning

confidence: 99%

“…For example, impairments have been seen on spatial, operant conditioning and context discrimination tasks (Bimonte-Nelson et al, 2003;Demas et al, 1996Demas et al, , 1998Escoriheula et al, 1995Escoriheula et al, , 1998Reeves et al, 1995;Seo and Isacson, 2005;Wenger et al, 2004), as well as on tasks involving sustained attention (Driscoll et al, 2004). However, learning and memory are not impaired in all tasks.…”

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

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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.

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“…In the frontal cortex, lower levels of BDNF with respect to diploid animals are found and negatively correlated with the progressive deterioration of working memory performance. 167 A major functional synaptic defect detectable in Ts65Dn mice is the failure to induce LTP in the hippocampus. [168][169][170][171] This deficit has been attributed to excessive inhibition, 171 a hypothesis recently confirmed by Fernandez et al, 172 which showed that the spatial learning disabilities observed in Ts65Dn mice are rescued by administration of non-competitive antagonists of GABAA receptors.…”

Section: Impact Of Ee On the Brain L Baroncelli Et Almentioning

confidence: 99%

Nurturing brain plasticity: impact of environmental enrichment

et al. 2009

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Environmental enrichment (EE) is known to profoundly affect the central nervous system (CNS) at the functional, anatomical and molecular level, both during the critical period and during adulthood. Recent studies focusing on the visual system have shown that these effects are associated with the recruitment of previously unsuspected neural plasticity processes. At early stages of brain development, EE triggers a marked acceleration in the maturation of the visual system, with maternal behaviour acting as a fundamental mediator of the enriched experience in both the foetus and the newborn. In adult brain, EE enhances plasticity in the cerebral cortex, allowing the recovery of visual functions in amblyopic animals. The molecular substrate of the effects of EE on brain plasticity is multi-factorial, with reduced intracerebral inhibition, enhanced neurotrophin expression and epigenetic changes at the level of chromatin structure. These findings shed new light on the potential of EE as a non-invasive strategy to ameliorate deficits in the development of the CNS and to treat neurological disorders.

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Frontal cortex BDNF levels correlate with working memory in an animal model of Down syndrome

Cited by 137 publications

References 52 publications

Search Strategies Used byAPPTransgenic Mice During Navigation in the Morris Water Maze

Search Strategies Used byAPPTransgenic Mice During Navigation in the Morris Water Maze

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

Nurturing brain plasticity: impact of environmental enrichment

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