ArticleNeurobiology of sleep and circadian rhythms2020
Suprachiasmatic lesions restore object recognition in down syndrome model mice.
Article in Neurobiology of sleep and circadian rhythms, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Circadian neurogenetics and its implications in neurophysiology, behavior, and chronomedicine.Neuroscience and biobehavioral reviews · 2024Review
- How did I come to sleep research and stay there?Sleep advances : a journal of the Sleep Research Society · 2024Article
- Reducing ER stress with chaperone therapy reverses sleep fragmentation and cognitive decline in aged mice.Aging cell · 2022Article
- Circadian clocks, cognition, and Alzheimer's disease: synaptic mechanisms, signaling effectors, and chronotherapeutics.Molecular neurodegeneration · 2022Review
- Hyper-Rigid Phasic Organization of Hippocampal Activity But Normal Spatial Properties of CA1 Place Cells in the Ts65Dn Mouse Model of Down Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Deletion of AMPA receptor GluA1 subunit gene (Gria1) causes circadian rhythm disruption and aberrant responses to environmental cues.Translational psychiatry · 2021Article
- Restoring the Molecular Clockwork within the Suprachiasmatic Hypothalamus of an Otherwise Clockless Mouse Enables Circadian Phasing and Stabilization of Sleep-Wake Cycles and Reverses Memory Deficits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Signalling pathways contributing to learning and memory deficits in the Ts65Dn mouse model of Down syndrome.Neuronal signaling · 2021Review
- Circadian Chimeric Mice Reveal an Interplay Between the Suprachiasmatic Nucleus and Local Brain Clocks in the Control of Sleep and Memory.Frontiers in neuroscience · 2021Article
- Suppression of Circadian Timing and Its Impact on the Hippocampus.Frontiers in neuroscience · 2021Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Ts65Dn mouse is a well-studied model of trisomy 21, Down syndrome. This mouse strain has severe learning disability as measured by several rodent learning tests that depend on hippocampal spatial memory function. Hippocampal long-term potentiation (LTP) is deficient in these mice. Short-term daily treatment with low-dose GABA receptor antagonists rescue spatial learning and LTP in Ts65Dn mice leading to the hypothesis that the learning disability is due to GABAergic over-inhibition of hippocampal circuits. The fact that the GABA receptor antagonists were only effective if delivered during the daily light phase suggested that the source of the excess GABA was controlled directly or indirectly by the circadian system. The central circadian pacemaker of mammals is the suprachiasmatic nucleus (SCN), which is largely a GABAergic nucleus. In this study we investigated whether elimination of the SCN in Ts65Dn mice would restore their ability to form recognition memories as tested by the novel object recognition (NOR) task. Full, but not partial lesions of the SCN of Ts65Dn mice normalized their ability to perform on the NOR test. These results suggest that the circadian system modulates neuroplasticity over the time frame involved in the process of consolidation of recognition memories.
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