Sternopygus macrurus of both sexes were injected with human chorionic gonadotropin (hCG) or saline. Electric organ discharge (EOD) frequency rose after hCG injections in females and gradually declined to baseline levels over the next few weeks. EOD changes in males were more complex and variable; most males showed an initial minor rise in EOD frequency followed by a larger decrease, or simply a decrease. hCG treatment also resulted in a rise in electroreceptor best frequency and shortened electric organ pulse duration in females, and had the opposite effect on these parameters in males. The saline-injected controls showed no changes in any of these parameters. Levels of testosterone (T) and 11-ketotestosterone, but not estrogen (E), were elevated in males preceding the fall in EOD frequency, whereas neither T nor E changed significantly in females before EOD frequency increases. Saline injections caused a drop in T in the male control group and had no effect in the female control group. We presume that the effect of hCG on the electrosensory system of males is mediated via androgens. Whether the effects of hCG on females are mediated by slight increases in circulating levels of gonadal steroids, the release of hormones other than T or E, or are due to direct effects on the nervous system is not known.

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Objective: Arl6ip1 has been reported to play a role in ocular development, but its regulatory function as it relates to proliferation is unclear. Therefore, this study aimed to evaluate how Arl6ip1 may regulate the proliferative behavior of retinal progenitor cells during zebrafish embryogenesis. Method: Arl6ip1 was specifically knocked down by introducing morpholino nucleic acid oligomers. The DNA content of cells dissociated from morphant eyes was analyzed by fluorescence-activated cell sorting (FACS). Retinal cells in the S- and late G2/M-phase were detected by labeling with BrdU and then immunostaining with anti-BrdU antibody and by immunostaining with phospho-histone H3 antibody, respectively. We also examined the expressions of shh,p57kip2, and cyclin D1 in retinas of experimental animals. The bidirectional plasmid pGFP:HSE:p57kip2 was used to rescue the defect in cell cycle exit. Results: FACS analysis showed that the >2C DNA content per cell in the eyes of arl6ip1 morphants was 2-fold greater than that of the wild type. Following functional Arl6ip1 knockdown, anti-BrdU- and anti-phospho-histone H3-positive signals were higher and the retinal progenitors kept expressing cyclin D1 but not shh or p57kip2, suggesting that eye progenitor cells remained in an early progenitor state and could not exit the cell cycle to progress to differentiation. Interestingly, overexpression of p57kip2, which enables exit from the cell cycle, led to a reduction of anti-BrdU-positive signals in the retinas of arl6ip1 morphants. Conclusion: Arl6ip1 not only affects signals controlling eye development but also plays an important role in the proliferation of retinal progenitor cells.