Meeting Abstract

P2.62  Friday, Jan. 4  Adrenergic regulation of effector function in the swimbladder of the zebrafish (Danio rerio) DUMBARTON, TC*; SMITH, FM; CROLL, RP; Dalhousie Univ. t.dumbarton@gmail.com

Inflation and deflation of the swimbladder in teleost fishes is thought to be mediated by the autonomic nervous system (ANS) acting on swimbladder effector tissues such as smooth muscle, vasculature and secretory cells. However, the effects of the neurotransmitters released from nerve terminals as well as the identity of post-junctional receptor subtypes are not well known. Previous studies in our laboratory have examined many aspects of the swimbladder in the teleost model, the zebrafish (Danio rerio), including its contribution to buoyancy, morphology and ontogeny. In addition, detailed anatomical studies have demonstrated the autonomic innervation of the organ, including the various neurotransmitter phenotypes present and the putative effectors such as smooth muscle and blood vessels. Here, we present indices of effector function from in situ and in vitro swimbladder tissue preparations in conjunction with pharmacological manipulations to demonstrate basic principles of swimbladder volume regulation. Initial studies have focused on the sympathetic branch of the ANS, where bath application of norepinephrine (NE) (1 x 10^-6 mol/L) evoked an increase in swimbladder internal pressure (204 � 29%; n=3), smooth muscle contraction, total volume decrease (26.7 � 5.4 %; n = 4) and gas expulsion through the pneumatic duct (5.6 � 0.93 μL; n = 5). NE and isoproterenol (a β-adrenergic agonist) evoked smooth muscle contraction in the circumferential smooth muscles of the anterior chamber of the swimbladder, but the α-adrenergic agonist phenylephrine had no effect. Our data thus suggest that β-adrenergic input into the swimbladder results in deflation reflexes that may be the principle means of decreasing fish buoyancy. Future studies will attempt to identify the processes involved in swimbladder inflation.