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© Uwe Maskos
Tranche d'hippocampe de souris colorée avec deux toxines spécifiques de sous-types de récepteur nicotinique, en rouge (grains), et en vert (corps cellulaires). L'hippocampe est la zone du cerveau qui gère la mémoire spatiale.
Publication : eLife

Alterations of specific cortical GABAergic circuits underlie abnormal network activity in a mouse model of Down syndrome.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in eLife - 12 Aug 2020

Zorrilla de San Martin J, Donato C, Peixoto J, Aguirre A, Choudhary V, De Stasi AM, Lourenço J, Potier MC, Bacci A,

Link to Pubmed [PMID] – 32783810

Link to DOI [DOI] – 10.7554/eLife.58731e58731

Elife 2020 Aug; 9():

Down syndrome (DS) results in various degrees of cognitive deficits. In DS mouse models, recovery of behavioral and neurophysiological deficits using GABAAR antagonists led to hypothesize an excessive activity of inhibitory circuits in this condition. Nonetheless, whether over-inhibition is present in DS and whether this is due to specific alterations of distinct GABAergic circuits is unknown. In the prefrontal cortex of Ts65Dn mice (a well-established DS model), we found that the dendritic synaptic inhibitory loop formed by somatostatin-positive Martinotti cells (MCs) and pyramidal neurons (PNs) was strongly enhanced, with no alteration in their excitability. Conversely, perisomatic inhibition from parvalbumin-positive (PV) interneurons was unaltered, but PV cells of DS mice lost their classical fast-spiking phenotype and exhibited increased excitability. These microcircuit alterations resulted in reduced pyramidal-neuron firing and increased phase locking to cognitive-relevant network oscillations in vivo. These results define important synaptic and circuit mechanisms underlying cognitive dysfunctions in DS.

https://pubmed.ncbi.nlm.nih.gov/32783810