Spatio-temporal patterns of pre- and postsynaptic inhibition were studied in the trigeminal spinal nucleus oralis of cats by means of systematic electrical stimulation of the facial skin. Stimulation of the facial skin induced an EPSP-IPSP sequence in trigemino-thalamic relay cells (TRC). The IPSP was depressed by picrotoxin but was resistant to strychnine. The largest IPSP was evoked from the center of the excitatory area, where stimulation induced the largest EPSP and spike potentials at the lowest intensity in the same TRC. The amplitude of the IPSP decreased with increasing distance from the center in parallel with that of the EPSP. In the great majority of trigeminal primary afferent fibers, the largest primary afferent depolarization (PAD) was not evoked from the center of the excitatory area, where the threshold for spike generation was lowest, but from the adjacent points on the face. Spike activities in a trigeminal primary afferent fiber did not evoke any detectable PAD in itself. The duration of the PAD was definitely longer than the IPSP in TRC. However, the temporal distribution of the peak of PADs was very similar to that of the EPSP in TRC. Inhibition was evoked in glutamate-induced spike discharges of TRC by stimulation of the points on the face, which were located close to the center of the excitatory area of the TRC. However, the afferent inhibition of both spontaneous and peripherally induced spike discharges of TRC outlasted the postsynaptic inhibition. Thus, the late phase of the afferent inhibition is most probably due to presynaptic inhibition. Presynaptic inhibition, together with postsynaptic inhibition, would be involved also in the early phase of afferent inhibition through its mutual inhibitory organization.