Do prostaglandins regulate external gill regression in anurans?
Although the endocrinological mechanism controlling regression of the internal, larval gills of anurans (frogs and toads) is well understood, the mechanism regulating loss of the external, embryonic gills is not known. Based on the homology of the mammalian ductus arteriosus with a portion of the amphibian branchial arches, and the regulation of blood flow in the mammalian ductus by prostaglandins of the E family (PGEs), we hypothesized that anuran external gill loss is also regulated by PGEs. To test this hypothesis, we topically applied both PGE2 and a synthetic analogue of PGE1, misoprostol, to embryos and young hatchlings of the red-eyed treefrog, Agalychnis callidryas. Both agents accelerated external gill regression. Furthermore, misoprostol overrode the inhibitory effect of hypoxia on gill regression in hatchlings and induced rapid loss of external gills in embryos, which normally maintain the gills until hatching. These observations support the hypothesis that PGEs regulate anuran external gill loss. The specific site of action for prostaglandins within the gills is not known; however, PGEs are secreted in the oral mucus of tadpoles, and this could be a natural topical source for these agents. PGEs offer a tool for manipulation of external gills and should facilitate tests of the physiological importance of these structures.
Warkentin
K M
KM
Smithsonian Tropical Research Institute, Balboa, Panama. kmwark2@pop.uky.edu
Wassersug
R J
RJ
D000222:Adaptation, Physiological; D000527:Alprostadil / Q000494:pharmacology*; D000818:Animals; D002025:Bufonidae / Q000196:embryology* / Q000502:physiology; D015232:Dinoprostone / Q000494:pharmacology*; D047108:Embryonic Development; D005880:Gills / Q000196:embryology*
D000527:Alprostadil; D015232:Dinoprostone