The effects of (+)-tubocurarine (TC) on single glutamate-activated channels in voltage-clamped locust muscle fibres have been examined using the patch-clamp technique. Glutamate alone produced a concentration-dependent increase in the probability of the channel being in the open state (po), but an increase in the concentration of glutamate (5×10−5-5×10−3 moll−1) in the presence of 5×10−4 moll−1 TC left po essentially unchanged. TC (5×10−6-5×10−4moll−1) caused a concentration- dependent decrease in the mean open time and in po for channels opened by 10−4 moll−4 glutamate. Correlations between successive openings and successive closings, which are characteristic of the kinetics of the muscle glutamate-receptorgated channel of locust muscle, were weakened in the presence of TC. There was little evidence of voltage sensitivity of TC action over the limited membrane potential (Vm) range −70 to −120 mV. The results are consistent with the idea that TC blocks the cation-selective channel gated by glutamate receptors in insect muscle and that the unblocking rate is low. They suggest also that block is at the level of the open channel, a conclusion supported by the wholly activation-induced depression of the neurally evoked twitch contraction of locust muscle by TC. Based upon a simple model for open channel block, TC is estimated to have a dissociation constant of 1.57 μmoll−1 (Vm = −100mV). The rate of association of blocker with channel is estimated to be 8.74×10−3ms−1(moll−1)−1 (Vm=−100mV). The rate of dissociation, estimated indirectly from the single-channel data, is 1.53×10−2ms−1, which gives a mean channel block time of 65.4 ms.