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In DS mouse models, recovery of behavioral and neurophysiological deficits using GABA\n                    <jats:sub>A<\/jats:sub>\n                    R 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.\n                  <\/jats:p>","DOI":"10.7554\/elife.58731","type":"journal-article","created":{"date-parts":[[2020,8,12]],"date-time":"2020-08-12T08:02:15Z","timestamp":1597219335000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.58731","source":"Crossref","is-referenced-by-count":43,"title":["Alterations of specific cortical GABAergic circuits underlie abnormal network activity in a mouse model of Down syndrome"],"prefix":"10.7554","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2848-7482","authenticated-orcid":true,"given":"Javier","family":"Zorrilla de San Martin","sequence":"first","affiliation":[{"name":"Institut du Cerveau (ICM), CNRS UMR 7225 \u2013 Inserm U1127, Sorbonne Universit\u00e9, Paris, 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