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Cited by 85Down syndrome and intellectual disability researchNeuroscience and Neuropharmacology ResearchGenetics and Neurodevelopmental Disorders

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

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Pérez-Cremades, D., Hernández, S., Blasco-Ibáñez, J. M., Crespo, C., Nacher, J., Varea, E.·2010·Journal of Neural Transmission
DOI 10.1007/s00702-010-0376-9
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Abstract

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.

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  • In Ts65Dn neocortex, there is an increase in the density of calretinin positive interneurons, no overall increase in parvalbumin interneurons, and altered distribution of both interneuron types throughout cortical layers.

    “another study found that there was an increase in the density of calretinin positive interneurons in the Ts65Dn neocortex and no overall increase in parvalbumin interneurons though the distribution of both interneurons types was significantly altered throughout the layers of the cortex (Pérez-Cremades et al., 2010).”

    From Neurodevelopment in Down syndrome: Concordance in humans and models (2022) · cites this paper as Pérez-Cremades et al., 2010

    The paper’s opening passage (p. 445) reports an increase in calretinin-immunoreactive cells in the somatosensory cortex of Ts65Dn mice. The available Results passage (p. 447) reports layer-specific changes for interneurons overall, but does not establish that parvalbumin interneurons showed no overall increase or that both named subtypes had significantly altered distributions across layers. (LLM, conf=0.76)

    Experimental — accuracy not yet measured

  • Striking conservation was found in the ratio of ExN:InN (2.17:1) and the ratio of MGE:CGE InNs (1.4:1) in both control and Ts21 samples.

    “Whereas Ts21 mouse models have identified alterations in the balance of ExN and InN (43-45), we found striking conservation in the ratio of ExN:InN (2.17:1) and the ratio of MGE:CGE InNs (1.4:1) in both control and Ts21 samples (Fig. 4B).”

    From Molecular and cellular processes disrupted in the early postnatal Down syndrome prefrontal cortex (2026) · cites this paper as [43]

    The Results (p. 447) report increased interneuron density in the somatosensory cortex of Ts65Dn mice, and the introduction (p. 446) discusses an imbalance of excitatory and inhibitory inputs. The paper does not measure an excitatory-to-inhibitory neuron ratio, so it supports the cited background point about altered inhibition but not the more specific claim about ExN:InN balance. The numerical ratios and their conservation are the citing authors’ own finding, not attributed to this source. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

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Authors
Pérez-Cremades, D., Hernández, S., Blasco-Ibáñez, J. M., Crespo, C., Nacher, J., & Varea, E.
Affiliations
Universitat de València (ES)
Corresponding author
Varea, E.
ORCID
Venue
Journal of Neural Transmission
Publisher
Springer Science and Business Media LLC
Published
2010-02-16
Volume
117
Issue
4
Pages
445-455
ISSN
  • 0300-9564 (ISSN-L)
  • 1435-1463
DOI
10.1007/s00702-010-0376-9
OpenAlex
W1968751712
Cited by
85
References
45
Citations by year
2026: 3 · 2025: 3 · 2024: 4 · 2023: 4 · 2022: 8 · 2021: 3 · 2020: 2 · 2019: 6 · 2018: 4 · 2017: 5 · 2016: 3 · 2015: 2 · 2014: 9 · 2013: 8 · 2012: 7
FWCI
9.24
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Neural Transmission (publishedVersion)
  • PubMed (publishedVersion)
  • LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc)
  • Repository of Digital Objects for Teaching Research and Culture (University of Valencia) (submittedVersion, other-oa)
Topics
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
Keywords
Down syndrome, Ts65Dn mouse model, somatosensory cortex, inhibitory interneurons, GAD67, synaptophysin, calretinin, dendritic branching, neuronal inhibition, epilepsy, intellectual disability
MeSH terms
Aging, Animals, Calcium-Binding Proteins, Cell Count, Disease Models, Animal, Down Syndrome, Glutamate Decarboxylase, Immunohistochemistry, Interneurons, Male, Mice, Transgenic, Neural Inhibition, Neural Pathways, Somatosensory Cortex, Synapses, Synaptophysin, Mice

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