Meeting Abstract

P2-140  Sunday, Jan. 5  Metabolism Sensing Mechanisms in the Electric Organ Cells of a Weakly Electric Fish NOURBAKHSH_REY, M*; MARKHAM, MR; The University of Oklahoma; The University of Oklahoma mrey@ou.edu

Weakly electric fish use electric organ discharges (EODs) produced by the coordinated action potentials of electric organ cells (electrocytes) to communicate and sense their environments. EOD production in Eigenmannia virescens incurs significant metabolic costs. During food restriction, these fish reduce EOD amplitude (EODa) to reduce metabolic costs, an effect mediated by leptin, a peptide hormone with multiple central and peripheral roles in energy homeostasis. We hypothesized that, in addition to central effects, leptin regulates EODa in E. virescens by directly regulating electrocytes. We found that electrocytes express a leptin receptor (LepR), supporting this hypothesis. Electrocytes also express ATP-sensitive K⁺ channels (K_ATP) that in many cell types are targeted by LepRs to couple electrical excitability to metabolic status. We therefore hypothesized that electrocyte LepRs would localize with K_ATP channels on the electrocyte’s anterior membrane. We expressed a red fluorescence-tagged LepR gene in electrocytes and found that LepRs are primarily expressed on the posterior membrane of electrocytes where voltage-gated Na⁺ channels (Na_v) and acetylcholine receptors (AchRs) are located, but more than 1 mm away from the electrocyte’s anterior membrane K_ATP channels. These findings suggest that leptin is instead modulating electrocyte function by targeting Na_v channels and/or AchRs to modulate their activity and/or membrane expression levels. We also investigated central hormonal networks that might interact with leptin to regulate EODa. Ghrelin hormones play important roles in energy homeostasis and are known to be regulated in part by leptin. In vivo injections of ghrelin increased EODa, suggesting that ghrelin is part of a central endocrine network that regulates EODa.