Evidence for GABA as an Inhibitory Neurotransmitter in the Neural Circuit Regulating Metamorphosis in the Marine Mollusc Ilyanassa obsoleta

Abstract

Event Abstract Back to Event Evidence for GABA as an Inhibitory Neurotransmitter in the Neural Circuit Regulating Metamorphosis in the Marine Mollusc Ilyanassa obsoleta Dhani Biscocho1 and Esther M. Leise1* 1 University of North Carolina Greensboro, Biology, United States The marine mud snail, Ilyanassa obsoleta, displays a biphasic life cycle. The initial phase consists of a larval stage in which the animals have ciliated feeding structures on the head (velar lobes) that allow them to swim weakly in the water column. The second phase consists of an adult stage during which the animals reside on intertidal mudflats as obligate omnivores. The event that links these life history stages is metamorphosis. Our interest lies in this transition from larva to non-reproductive adult, the neural circuit that controls metamorphosis, and the cues which are responsible for initiating this process. Molluscan metamorphosis requires multiple changes in cellular action, morphology, physiology and behavioral interactions. I. obsoleta undergoes transformations that include loss of one brain ganglion (the apical ganglion), reorganization of other brain regions, and disappearance of the velar lobes. The neurotransmitter γ-aminobutyric acid (GABA) can induce metamorphosis in a related mollusc, the abalone Haliotis rufescens (Morse, et al. 1979, Science 204, 407-410), but results of our experiments with I. obsoleta have revealed an inhibitory action for GABA. Bath application of GABA to metamorphically competent larvae of I. obsoleta does not elicit metamorphosis. However, exposure of larvae to seawater with reduced chloride concentrations induced metamorphosis in a dose-dependent fashion. Earlier work on I. obsoleta has demonstrated that the neurotransmitters serotonin (5-HT) and nitric oxide function as a promoter and repressor of metamorphosis, respectively. GABA can inhibit serotonergically induced metamorphosis, suggesting that GABA acts either downstream of, or directly on serotonergic neurons. We are currently exploiting reagents that modify the function of GABA transport, synthesis and metabolism to verify that GABA has a role in this system. In bath application, muscimol, a GABA-A agonist, inhibits spontaneous larval metamorphosis for 48 hours. Bath application of isoguvacine, another GABA-A agonist or aminooxyacetic acid (AOA), a major inhibitor of GABA-Transaminase can also repress metamorphosis in 5-HT-induced larvae. In current experiments, we are injecting reagents into competent larvae to decrease chances of interactions between neuroactive compounds and epidermal sensory receptors. These experiments should further support the idea that GABAergic activity occurs internally within the larval central nervous system, perhaps in the apical ganglion. Together, our data will help to elucidate the role of GABA in this molluscan metamorphic pathway. Acknowledgements Funded in part by UNCG Department of Biology Keywords: GABA, gastropod, Larva, metamorphosis, mollusc, Nitric Oxide, Serotonin, Snail Conference: Tenth International Congress of Neuroethology, College Park. Maryland USA, United States, 5 Aug - 10 Aug, 2012. Presentation Type: Poster Presentation (see alternatives below as well) Topic: Development Citation: Biscocho D and Leise EM (2012). Evidence for GABA as an Inhibitory Neurotransmitter in the Neural Circuit Regulating Metamorphosis in the Marine Mollusc Ilyanassa obsoleta. Conference Abstract: Tenth International Congress of Neuroethology. doi: 10.3389/conf.fnbeh.2012.27.00131 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 26 Apr 2012; Published Online: 07 Jul 2012. * Correspondence: Dr. Esther M Leise, University of North Carolina Greensboro, Biology, Greensboro, NC, 27412, United States, esther_leise@uncg.edu Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. 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