Weakly electric fish emit electric organ discharges (EODs) to locate objects around themselves and for communication. The EOD is generated by a simple hierarchically organized, neurophysiologically accessible circuit, the electromotor system. A number of forms of plasticity of the EOD waveform are initiated by social or environmental factors and mediated by hormones or neurotransmitters. Because the behavior itself is in the form of electric discharges, behavioral observations easily lead to testable hypotheses about the biophysical bases of these plasticities. This allows us to study ionic channels in their native cellular environments, where the regulation of various parameters of these currents have obvious functional consequences. In this review, we discuss three types of plasticity: a rapidly occurring, long-lasting, N-methyl-d-aspartate (NMDA)-receptor-dependent increase in baseline firing frequency of neurons in the pacemaker nucleus that underlies a readjustment of the baseline EOD frequency after long bouts of the jamming avoidance response; a rapidly occurring diurnal change in amplitude and duration of the EOD pulse that depends in part on modulation of the magnitude of the electrocyte Na+ current by a protein kinase; and a slowly occurring, hormonally modulated tandem change in pacemaker firing frequency and in the duration of the EOD pulse in which changes in EOD pulse duration are mediated by coordinated shifts in the activation and inactivation kinetics of the electrocyte Na+ and K+ currents.

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