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Hippocampal hypocellularity in the Ts65Dn mouse originates early in development.

Hernan A Lorenzi1, Roger H Reeves

  • 1Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2185, USA.

Brain Research
|July 11, 2006
PubMed
Summary

Ts65Dn mice, a model for Down syndrome, exhibit early hippocampal granule cell deficits. These developmental changes, present at postnatal day 6, contribute to cognitive impairments in trisomic mice.

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Genetics

Background:

  • Ts65Dn mice model Down syndrome, exhibiting trisomy for mouse chromosome 16 segments orthologous to human chromosome 21.
  • These mice display learning and memory deficits, particularly in hippocampal-dependent tasks.
  • Previous research noted hippocampal structural abnormalities in aged Ts65Dn mice, but the developmental origin was unclear.

Purpose of the Study:

  • To investigate whether hippocampal abnormalities in Ts65Dn mice originate during development or are secondary to age-related neurodegeneration.
  • To quantitatively assess hippocampal volume and neuron numbers in young and adult Ts65Dn mice.

Main Methods:

  • Utilized the optical fractionator method for quantitative stereological analysis.
  • Examined hippocampal volume and neuron counts in young (postnatal day 6) and adult (3-month-old) Ts65Dn mice and euploid littermates.

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Main Results:

  • Young Ts65Dn mice (P6) had 20% fewer dentate gyrus granule cells compared to euploid controls.
  • A significant reduction (18%) in mitotic cells was observed in the granule cell layer and hilus of P6 Ts65Dn mice.
  • Granule cell hypocellularity in Ts65Dn mice persisted into adulthood, preceding cholinergic neuron degeneration.

Conclusions:

  • Hippocampal hypocellularity in Ts65Dn mice originates early in development.
  • These early developmental deficits in granule cell numbers may underlie cognitive impairments observed in this Down syndrome model.