Objective Peroxynitrite (ONOO-), which formed in vivo under the oxidative stress in a diffusion-controlled reaction between nitric oxide (NO) and superoxide anion, is a strong oxidizing and nitrating agent to mediate much of the toxicity of NO.It has been suggested that this kind of deleterious reactive nitrogen species (RNS) was involved in the development of a variety of pathological conditions such as the neurodegenerative disorders with disrupted memory and impaired cognition.The aim of this study was to investigate actions of ONOO-on synaptic transmission in hippocampal CA1 neurons of Wistar rats.Methods Using patch clamp methods, we made the recording of NMDA-mediated miniature glutamatergic excitatory postsynaptic currents (mEPSC) and AMPA-mediated mEPSC in the hippocampal neurons in CA1 area of Wistar rats.Results Our results demonstrated that SIN-1 (3-morpholino-sydnonimine), used as the donor of ONOO-, induced a bidirectional modulation of glutamatergic transmission under different concentrations.A high dose (1 mM) of SIN-1 decreased amplitudes of both NMDA-and AMPA-mediated mEPSC, mainly through altering the NMDA-mEPSC.And lower dose (100 μM) of SIN-1 caused a consistent increase in amplitudes of AMPA-and NMDA-mediated mEPSC, but depressed the frequencies.Additionally, co-treatment with SIN-1 and uric acid, a perxynitite scavenger, had no effects on mEPSC.Conclusion The results suggested that perxynitite could induce neurotoxicity through modulating excitatory transmitter release in both presynaptic and postsynaptic ways and play a role in the modification of synaptic function in hippocampal CA1 neurons.