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Nevertheless, the specific timing of the impact of oxytocin on social behavior has remained unclear. Using mouse strains from oxytocin\u2010Cre mice crossed with Cre\u2010dependent chemogenetic mice, oxytocinergic neuronal activity is selectivity manipulated during the early or late postnatal stages and revealed, for the first time, that the suppression of oxytocinergic neurons in the early rather than late postnatal stage led to the emergence of autistic\u2010like behaviors. Notably, significantly reduced oxytocin levels are identified specifically during the early postnatal stage in both valproic acid (VPA)\u2010exposed and <jats:italic>Fmr1<\/jats:italic>\u2010KO mouse brains, along with an impairment of the GABA reversal potential and downregulation of the Na<jats:sup>+<\/jats:sup>\u2010K<jats:sup>+<\/jats:sup>\u20102Cl<jats:sup>\u2212<\/jats:sup> cotransporter (NKCC1) post\u2010birth. 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