Exaggerated responses to sensory stimuli is a hallmark of Fragile X syndrome (FXS), contributes to, inattention, anxiety, and learning challenges. Such sensory hypersensitivity are recapitulated in the Fmr1 knockout (KO). Recent studies in Fmr1 KO mice have demonstrated differences in GABAergic inhibition, including activity of cortical interneurons as well as a delayed switch in the polarity of GABA signaling during development. Previously, we found that administration of bumetanide to block the chloride (Cl-) transporter NKCC1, could rescue synaptic circuit phenotypes in primary somatosensory cortex (S1) of juvenile and adultFmr1 KO mice. However, it remains unknown whether bumetanide can rescue earlier circuit or behavioral phenotypes in neonatal Fmr1 KO mice. Here, we targeted NKCC1 by both acute and chronic administration of bumetanide in Fmr1 KO mice and performed in vivo 2-photon calcium imaging to record neuronal activity. We demonstrate that layer (L) 2/3 pyramidal cells in S1 of Fmr1 KO mice show a higher frequency of synchronous events at postnatal day (P) 6 compared to wild-type controls. This was reversed by acute administration of bumetanide at P6. Furthermore, chronic administration of bumetanide restored S1 circuit differences in Fmr1 KO mice, including reduced adaptation of L2/3 neurons to repetitive whisker stimulation and ameliorated behavioral tactile defensiveness. Chronic bumetanide treatment also rectified the reduced feedforward GABAergic inhibitory currents in S1 L2/3 neurons. This further supports the notion that synaptic, circuit, and sensory behavioral phenotypes in Fmr1KO can be mitigated by inhibitors of NKCC1, such as the FDA-approved diuretic bumetanide.