Regulation of electrical excitability : individual, gender and hormonally-induced variation in potassium channel expression in the electric organ

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2003-05

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Few, William Preston, 1974-

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Abstract

The regulation of electrical excitability is a critical component of neuronal plasticity. The cells of the electric organ (electrocytes) of the weakly electric fish Sternopygus exhibit variation in excitability that underlies an individually distinct, sexually dimorphic communication signal called the electric organ discharge (EOD). The EOD is sinusoidal, ranges in frequency from 30-200 Hz, and is modulated by steroid hormones. The frequency of the EOD is set by the cells of a medullary pacemaker nucleus. The EOD pulse duration, which is negatively correlated with EOD frequency, is determined by the excitability of the electrocytes. This dissertation focuses on how variation in electrocyte excitability can arise, and is divided into two parts. The first part demonstrates, using small doses of the androgen dihydrotestosterone (DHT) implanted in the electric organ, that androgens can broaden EOD pulse duration despite a stable pacemaker nucleus firing frequency. Using immunocytochemistry, it is shown that electrocytes possess androgen receptors. Together these experiments suggest that androgens may act on the electrocytes to increase EOD pulse duration, and therefore play a causative role in determining electrocyte excitability. The second part of this dissertation focuses on the voltage-dependent K+ channels expressed in the electric organ. Since electrocyte K+ current kinetics covary with EOD frequency, we hypothesized that the differential expression of K+ channels may underlie variation in electrocyte excitability. To test this, we cloned Kv1 channels from the electric organ and assayed their levels of mRNA expression across the EOD frequency range. Kv1.1 and Kv1.2a expression is higher in high frequency, female electric organs (which have fast current kinetics) than in low frequency, male electric organs. Kv1.2b expression in the electric organ does not correlate with EOD frequency. To test whether Kv1 expression is modulated by steroid hormones, individuals were treated with DHT or human chorionic gonadotropin (hCG), which increases or decreases EOD pulse duration, respectively. DHT decreased Kv1.1 and Kv1.2a, but not Kv1.2b, expression. hCG increased Kv1.2a, but not Kv1.1 or Kv1.2b expression. Thus, individual, sex, and hormonally-induced differences in the expression of Kv1 K+ channels play a critical role in determining electrocyte excitability.

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