Meeting Abstract
Signal plasticity can maximize the utility of costly animal signals. This is especially true for multi-functional signals such as the electric organ discharges (EODs) of weakly electric fishes. How this plasticity affects the functional and behaviorally relevant properties of animal signals is not fully understood. We compared signal plasticity in four species of Brachyhypopomus, a genus of weakly electric fishes (Gymnotiformes, Hypopomidae). Regulated by adrenocorticotropic hormone (ACTH), this type of EOD plasticity allows some species to increase their EOD amplitude in response to circadian cues and social stimuli. ACTH-induced amplitude changes occur via different mechanisms, possibly the rapid trafficking of ion channels to the membranes of the electrocytes (electric organ cells), or by regulating ion channel kinetics. We used in vivo injections and in vitro electrophysiology to study the effects of ACTH on the behavior of whole fish and individual electrocytes. We also used immunolocalization to map the distribution of ion channels within electrocytes, which contributes to the species-specific EOD waveform. We predicted that the monophasic species, B. bennetti, would show increased EOD amplitude plasticity relative to congeners with biphasic EODs. We further predicted that voltage-gated sodium channels would only be present on the innervated posterior membrane as in another monophasic gymnotiform, the Electric Eel. Surprisingly, B. bennetti shows significantly less EOD amplitude plasticity compared to closely related biphasic species. Further, we found that sodium channels are present on both electrocyte membranes and that a second action potential drastically reduces the overall head-positive current, likely at great metabolic cost.
