Meeting Abstract
P2.10 Tuesday, Jan. 5 Evidence for evolutionary reductions in both the ligand and receptor that regulate rapid skin darkening in the Texas toad, Bufo speciosus. KUMAR, A.; LARSON, R.; BROWN, C.; CARR, J.A.*; Texas Tech Univ., Lubbock; Texas Tech Univ., Lubbock; Texas Tech Univ., Lubbock; Texas Tech Univ., Lubbock james.carr@ttu.edu
Two mechanisms regulate skin darkening in the South African clawed frog Xenopus laevis: a rapid response mediated by beta-adrenergic receptors on melanophores and a slower more sustained skin darkening resulting from MSH. Presumably these pathways have evolved as a response to predation, however it is unclear how these pathways operate in anuran species that would derive no benefit from the ability to mount a rapid melanophore response. Bufo speciosus, the Texas toad, is a desert adapted species that is nocturnal during the spring and summer but estivates underground the rest of the year. Compared to X. laevis, skin darkening is much slower and not as pronounced in B. speciosus. The dopamine neurotoxin 6-OHDA produced skin darkening in B. speciosus that amounted to 85% of the maximum achieved during long term dark adaptation. The dopamine receptor antagonist haloperidol had no effect while administration of the dopamine receptor agonist apomorphine significantly reduced skin darkening. Interestingly B. speciosus exhibited a strongly attenuated response to isoproterenol compared to X. laevis, and skin darkening in white adapted Bufo after transfer to a dark background was not affected by propranolol. To investigate the basis for the lack of response to beta-adrenergic agents, we examined differences in beta-adrenergic binding sites and skin catecholamine content between the two species. Skin from X. laevis had significantly more [3H]dihydroalprenolol binding sites as well as greater amounts of both dopamine and epinephrine compared to skin from B. speciosus. We conclude that B. speciosus appears to lack a mechanism for rapid skin darkening due to reductions in both the ligand and receptor controlling this response.
