Meeting Abstract
Male Anolis sagrei erect a vertical ridge of tissue along their neck and spine during escalated aggressive encounters with other males. The function of the crest erection is thought to modify the lateral profile of a fighting male, suggesting an important behavioral cue. However, very little is known regarding the physiological and cellular regulation of crest development. Previous work in our lab has shown that the β-adrenergic receptor (BAR) agonist isoproterenol produces crest erections and the BAR antagonist propranolol inhibits crest formation. We found that pharmaceuticals developed for specific mammalian α- and β-receptors had varying efficacies on the Anolis receptors. For example, salbutamol, a β-2 agonist, induced crest formation, but terbutaline failed. The α-1 agonist methoxamine inhibited β-stimulated crest formation, while phenylephrine occasionally induced a crest. To understand the intracellular mechanisms involved in crest formation, we used the forskolin analog NKH-477 to increase intracellular cAMP. Systemic injections of NKH-477 induced full crest formation, while small volume injections directly into the crest produced a localized, partial crest at the injection site. Based on these results in combination with our histological examinations, we hypothesize that BAR stimulation of vascular smooth muscle increases intracellular cAMP, which causes vasodilation of vessels within the crest organ. Further, we hypothesize that leaky capillaries within the crest allow fluid to leave the blood vessels and this increases the extracellular fluid volume that causes dorsal crest erection.
