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To investigate underlying neuronal processing defects located in the auditory cortex (AC), we performed two-photon Ca<jats:sup>2+<\/jats:sup>imaging in<jats:italic>FMR1<\/jats:italic>(<jats:italic>fragile X messenger ribonucleoprotein<\/jats:italic><jats:italic>1<\/jats:italic>) knock-out (KO) mice, a model for fragile X syndrome (FXS), the most common cause of hereditary ASD in humans. For primary AC (A1) and the anterior auditory field (AAF), topographic frequency representation was less ordered compared with control animals. We additionally analyzed ensemble AC activity in response to various sounds and found subfield-specific differences. In A1, ensemble correlations were lower in general, while in secondary AC (A2), correlations were higher in response to complex sounds, but not to pure tones. Furthermore, sound specificity of ensemble activity was decreased in AAF. Repeating these experiments 1\u2005week later revealed no major differences regarding representational drift. Nevertheless, we found subfield- and genotype-specific changes in ensemble correlation values between the two times points, hinting at alterations in network stability in<jats:italic>FMR1<\/jats:italic>KO mice. 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