The effects of anaesthesia with etomidate on the cellular mechanisms of sensory processing and sensorimotor coordination have been investigated in the active electric sense of the mormyrid fish Gnathonemus petersii. Like many anaesthetics, etomidate is known to potentiate GABA_A receptors but little is known about the effects on sensory processing at the systems level. A better understanding is necessary for experimental studies of sensory processing, in particular regarding possible effects on the dynamic structure of excitatory and inhibitory receptive fields and to improve the knowledge of the mechanisms of anaesthesia in general. Etomidate slowed the electromotor discharge rhythm, probably due to feedback inhibition at the premotor level, but did not alter the structure of the electromotor command. Sensory translation through primary afferents projecting to the cerebellum-like electrosensory lobe (ELL) was not changed. However, central interneurons and projection neurons were hyperpolarized under etomidate and their spiking activity was reduced. Although the spatial extent and the centre/surround organization of sensory receptive fields were not changed, initial excitatory responses were followed by prolonged inhibition. Corollary discharge input to ELL was maintained and the temporal sequence of excitatory and inhibitory components of this descending signal remained intact. Later inhibitory corollary discharge responses were prolonged by several hundred milliseconds. The result was that excitatory reafferent sensory input was conserved with enhanced precision of timing, while background activity was greatly reduced. Anti-Hebbian synaptic plasticity evoked by association of sensory and corollary discharge input was still present under anaesthesia, and differences compared with the non-anaesthetised condition are discussed.