{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T05:17:48Z","timestamp":1791091068630,"version":"4.1.0"},"reference-count":42,"publisher":"National Academy of Sciences","issue":"45","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2013,11,5]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    Advances in human genetics have identified many gene alterations that cause autism, but how these mutations lead to cortical dysfunction is not understood. Mutations in the gene phosphatase and tensin homolog on chromosome ten (\n                    <jats:italic>PTEN<\/jats:italic>\n                    ) cause autism and intellectual disability. We have discovered that single-copy deletion of\n                    <jats:italic>Pten<\/jats:italic>\n                    results in overexpression of the small-conductance calcium-activated potassium channel in cortical neurons. This overexpression leads to decreased sensitivity of cortical neurons to incoming inputs. In vivo, this diminished excitability leads to decreased primary visual cortical responsiveness to visual stimuli. We hypothesize that diminished cortical responses in primary sensory regions lead to poor recruitment of secondary sensory cortices, leading to sensory processing deficits. Our findings identify a unique target for potential pharmacological intervention.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1309207110","type":"journal-article","created":{"date-parts":[[2013,10,21]],"date-time":"2013-10-21T22:57:55Z","timestamp":1382396275000},"page":"18297-18302","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":44,"title":["Overexpression of calcium-activated potassium channels underlies cortical dysfunction in a model of\n                    <i>PTEN<\/i>\n                    -associated autism"],"prefix":"10.1073","volume":"110","author":[{"given":"Pablo","family":"Garcia-Junco-Clemente","sequence":"first","affiliation":[{"name":"Departments of aNeurobiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David K.","family":"Chow","sequence":"additional","affiliation":[{"name":"Departments of aNeurobiology 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