Meeting Abstract
Weakly electric fish navigate and communicate with electric organ discharges (EODs) produced by the coordinated action potentials of muscle-derived electric organ cells (electrocytes). EOD production incurs significant metabolic costs in the electric fish Eigenmannia virescens which reduces signal amplitude during food restriction. This effect is mediated by leptin, a peptide hormone that typically plays multiple central and peripheral roles in energy homeostasis. We hypothesized that, in addition to these functions, leptin is also regulating EOD amplitude in E. virescens by directly modulating electrocyte function. We found that electrocytes express a leptin receptor (LepR), and gene phylogeny groups the E. virescens LepR with those of freshwater teleost fish. Electrocytes also express an ATP-sensitive K+ channel (KATP) complex that couples electrical excitability to metabolic status in a number of cell types including smooth and skeletal muscle. In many cases KATP is a downstream target of leptin. We cloned electrocyte KATP subunits and expressed them in Xenopus oocytes. Voltage-clamp experiments revealed an inwardly rectifying K+ conductance that is enhanced by the metabolic inhibitor sodium azide. Gene phylogeny of E. virescens KATP indicates that the functional channel consists of Kir6.2 and SUR2B subunits. Because leptin receptors are known to be coupled to KATP channels in several other physiological systems, we hypothesize that electrocyte LepR and KATP channels form a signaling complex that couples metabolic state to signal output in E. virescens. Future experiments will test this hypothesis.
