Details

Autor(en) / Beteiligte

• Wicher, Dieter
• Agricola, Hans-Jurgen
• Sohler, Sandra
• Gundel, Matthias
• Heinemann, Stefan H
• Wollweber, Leo
• Stengl, Monika
• Derst, Christian

Titel

Differential Receptor Activation by Cockroach Adipokinetic Hormones Produces Differential Effects on Ion Currents, Neuronal Activity, and Locomotion

Ist Teil von

• Journal of neurophysiology, 2006-04, Vol.95 (4), p.2314-2325

Ort / Verlag

United States: Am Phys Soc

Erscheinungsjahr

2006

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• 1 Department of Neurohormones, Saxon Academy of Sciences, Jena 2 Institute of Zoology, Friedrich Schiller University, Jena 3 Institute of Animal Physiology, Philipps University Marburg, Marburg 4 Institute of Molecular Cell Biology, Medical Faculty of the Friedrich Schiller University, Jena 5 Institute of Molecular Biotechnology, Jena 6 Center for Anatomy, Charité Berlin, Berlin, Germany Submitted 29 September 2005; accepted in final form 28 November 2005 Adipokinetic hormone (AKH) peptides in insects serve the endocrine control of energy supply. They also produce, however, neuronal, vegetative, and motor effects, suggesting that AKHs orchestrate adaptive behavior by multiple actions. We have cloned, for Periplaneta americana , the AKH receptor to determine its localization and, based on current measurements in neurons and heterologous expression systems, the mechanisms of AKH actions. Apart from fat body, various neurons express the AKH receptor, among them abdominal dorsal unpaired median (DUM) neurons, which release the biogenic amine octopamine. They are part of the arousal system and are involved in the control of circulation and respiration. Both the two Periplaneta AKHs activate the G s pathway, and AKH I also potently activates G q . AKH I and—with much less efficacy—AKH II accelerate spiking of DUM neurons through an increase of the pacemaking Ca 2+ current. Because the AKHs are released from the corpora cardiaca into the hemolymph, they must penetrate the blood-brain barrier for acting on neurons. That this happens was shown electrophysiologically by applying AKH I to an intact ganglion. Systemically injected AKH I stimulates locomotion potently in striking contrast to AKH II. This behavioral difference can be traced back conclusively to the different effectiveness of the AKHs on the level of G proteins. Our findings also show that AKHs act through the same basic mechanisms on neuronal and nonneuronal cells, and they support an integration of metabolic and neuronal effects in homoeostatic mechanisms. Address for reprint requests and other correspondence: D. Wicher, Max Planck Institute for Chemical Ecology, Hans-Knöll-Str. 8, 07745 Jena, Germany (E-mail: dwicher{at}ice.mpg.de )