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Suprachiasmatic lesions restore object recognition in down syndrome model mice. | LitMetric

Suprachiasmatic lesions restore object recognition in down syndrome model mice.

Neurobiol Sleep Circadian Rhythms

Biology Department, 371 Serra Mall, Stanford University, Stanford, CA, 94305-5020, USA.

Published: May 2020

AI Article Synopsis

  • - The Ts65Dn mouse model exhibits severe learning disabilities associated with trisomy 21 (Down syndrome) due to impaired hippocampal function, particularly long-term potentiation (LTP).
  • - Treatment with low-dose GABA receptor antagonists significantly improves spatial learning and LTP in these mice, indicating that the learning issues may stem from excessive inhibition in hippocampal circuits modulated by the circadian system.
  • - Lesioning the suprachiasmatic nucleus (SCN), the primary circadian pacemaker, fully restores recognition memory abilities in Ts65Dn mice, highlighting the interaction between circadian rhythms and neuroplasticity related to memory consolidation.

Article 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7075983PMC
http://dx.doi.org/10.1016/j.nbscr.2020.100049DOI Listing

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