Redox signaling regulates neuronal function, yet how acute cell-specific hydrogen peroxide (HO) elevation affects hippocampal network oscillations remains unclear. Using a chemogenetic approach in mouse hippocampal slices and in vivo, we induced controlled intracellular HO production selectively in pyramidal cells or interneurons and examined the effects on sharp-wave ripples (SPW-Rs) and gamma oscillations. Pyramidal-cell HO reduced SPW-R amplitude, propagation success, and CA3-CA1 synchrony, accompanied by a reversible 25% reduction in EPSC amplitude without affecting IPSCs or paired-pulse ratios, indicating a postsynaptic mechanism. Interneuron-specific HO reduced SPW-R frequency and propagation success without altering propagation velocity. In striking contrast, gamma oscillations, whether evoked optogenetically in slices or recorded spontaneously in vivo, were resistant to HO elevation regardless of cell type targeted. These findings reveal that SPW-Rs and gamma oscillations exhibit differential sensitivity to acute HO, with cell-type-specific effects on ripples but universal resistance of gamma activity. Because the two rhythms support distinct cognitive operations, this dissociation suggests that transient redox signals may selectively constrain memory consolidation while leaving active encoding-related processing intact, and that the cellular source of HO determines which network state is affected.