Abstract

Event Abstract Back to Event Inhibition of a CPG: Investigating Descending Control Karen J. Thompson1* 1 Agnes Scott College, Biology, Neuroscience Program, United States Central pattern generators (CPGs) may be spontaneously active (e.g. respiration), initiated by excitatory neural inputs (e.g. locomotion), or much more rarely activated by removing tonic inhibition (e.g. ejaculation). In insects, CPGs control several behaviors produced by terminal abdominal segments, including copulation in male mantids, stinging in honeybees, and grasshopper oviposition. Multiple lines of evidence point to a mechanism there of neural control based upon “release” from descending inhibition. We have utilized lesions and pharmacological tools to investigate the mechanism whereby higher centers of the nervous system control the oviposition CPG in grasshoppers. For all experiments, CPG activity was monitored electromyographically and a preparation of consisting of metathoracic ganglion through terminal abdominal ganglion, in situ, was used. These preparations are quiescent. However, once the nerve cord was transected below the metathoracic ganglion, the oviposition CPG in females, or the corresponding motor program in male homologues, was induced. In this system nerve cord transection activates the motor program 100% of the time. These results indicate that neurons located in the metathoracic ganglionic mass, not in the brain or suboesophageal ganglion, provide the key descending input. Decapitation only induces a transient and irregular expression of the oviposition pattern. Because the fast inhibitory neurotransmitters of arthropods are GABA (gamma-amino butyric acid) and histamine, we use pharmacological tools to test predictions from the hypothesis that neural inhibition provided by GABAergic or histaminergic neurons provided the descending control of oviposition. We bath-applied these compounds and their agonists and antagonists to terminal segments in animals before and after nerve cord transection. The motor pattern was initiated in intact preparations by application of the chloride channel blocker picrotoxin. The motor pattern was also initiated by application of the specific histamine H2-receptor antagonist (ranitidine), but not by the GABAA receptor antagonist (bicuculline). After the nerve cord was transected below the metathoracic ganglion and the CPG was active, the pattern was inhibited by HA application but not by GABA. Washout reversed all pharmacological effects. Furthermore, when the intact nerve cord was cut in the presence of bath-applied histamine, the CPG failed to activate. Drug concentrations necessary were high, in the range of 1 mM, but were lower (0.1 mM) with desheathed preparations or younger adults. These results are consistent with previous transection, cold-block, and stimulation studies which indicated that the oviposition CPG was activated by release from tonic descending inhibition. The descending neurons appear to exert their inhibitory effect through histaminergic receptor chloride channels. Backfill studies have revealed descending neurons with primarily contralateral cell bodies in the metathoracic and abdominal neuromeres of the metathoracic ganglionic mass. The largest collection is located in the first abdominal neuromere. Evidence from the literature has indicated the presence of a limited number of ascending segmentally repeated histamine-positive cells in the ventral nerve cord. We are continuing our investigation to reconcile this observation with our prediction of descending histaminergic neurons. Acknowledgements Supported by NIH EARDA #HD054966-04. Keywords: central pattern generator, descending control, GABA, Histamine, insect, Oviposition 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: Motor Systems Citation: Thompson KJ (2012). Inhibition of a CPG: Investigating Descending Control. Conference Abstract: Tenth International Congress of Neuroethology. doi: 10.3389/conf.fnbeh.2012.27.00330 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: 30 Apr 2012; Published Online: 07 Jul 2012. * Correspondence: Prof. Karen J Thompson, Agnes Scott College, Biology, Neuroscience Program, Decatur, GA, 30030, United States, kthompson@agnesscott.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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