The pair of giant reciprocally coupled neurons VD1 and RPaD2 within the CNS of the freshwater pond snail Lymnaea stagnalis was used to analyse the effect of hydrogen peroxide on gap-junction connection. Electrical activity of VD1/RPaD2 was recorded with intracellular microelectrodes in order to analyse gap-junction signalling. Hydrogen peroxide application (1 × 10−4 M) results in a rapid, 1.3-fold, increase in VD1/RPaD2 spiking frequency within 30 s after application. This was accompanied by a slight reduction in action potential amplitude. In addition, H2O2 induced a significant reduction in the steady-state bidirectional coupling ratio between the neurons. The maximal reduction in the coupling ratio, 1.8–1.9 fold, was measured 3 min after H2O2 application. However, the network input resistance did not undergo a detectable change. The voltage-gated Ca2+ channel blocker, nifedipine (1 × 10−4 M), abolished the effect of H2O2 on the coupling ratio and firing frequency. All the effects of H2O2 were reversible, that is, washing the preparation with standard physiological saline restored the properties of the neuronal coupling to the pre-treatment value. These data are consistent with a dynamic modulation of the gap-junction properties by H2O2 between these two neurons.