Original Research Article
The satiety signaling neuropeptide perisulfakinin inhibits the activity of central neurons promoting general activity
Dieter Wicher 1*, Christian Derst 2, Hélène Gautier 3, Bruno Lapied 3, Stefan H. Heinemann 4 and Hans-Jürgen Agricola 5
1 Department of Evolutionary Neuroethology, Max Planck Institute for Chemical Ecology, Germany
2 Center for Anatomy, Germany
3 Laboratoire Récepteurs et Canaux Ioniques Membranaires, RCIM, Université d’Angers, France
4 Department of Biophysics, Center for Molecular Biomedicine , Friedrich Schiller University Jena, Germany
5 Center for Molecular Biomedicine, Friedrich Schiller University Jena, Germany
2 Center for Anatomy, Germany
3 Laboratoire Récepteurs et Canaux Ioniques Membranaires, RCIM, Université d’Angers, France
4 Department of Biophysics, Center for Molecular Biomedicine , Friedrich Schiller University Jena, Germany
5 Center for Molecular Biomedicine, Friedrich Schiller University Jena, Germany
The metabolic state is one of the determinants of the general activity level. Satiety is related to resting or sleep whereas hunger correlates to wakefulness and activity. The counterpart to the mammalian satiety signal cholecystokinin (CCK) in insects are the sulfakinins. The aim of this study was to resolve the mechanism by which the antifeedant activity of perisulfakinin (PSK) in Periplaneta americana is mediated. We identified the sources of PSK which is used both as hormone and as paracrine messenger. PSK is found in the neurohemal organ of the brain and in nerve endings throughout the central nervous system. To correlate the distributions of PSK and its receptor (PSKR), we cloned the gene coding for PSKR and provide evidence for its expression within the nervous system. It occurs only in a few neurons, among them are the dorsal unpaired median (DUM) neurons which release octopamine thereby regulating the general level of activity. Application of PSK to DUM neurons attenuated the spiking frequency (EC50=11pM) due to reduction of a pacemaker Ca2+ current through cAMP-inhibited pTRPγ channels. PSK increased the intracellular cAMP level while decreasing the intracellular Ca2+ concentration in DUM neurons. Thus, the satiety signal conferred by PSK acts antagonistically to the hunger signal, provided by the adipokinetic hormone (AKH): PSK depresses the electrical activity of DUM neurons by inhibiting the pTRPγ channel that is activated by AKH under conditions of food shortage.
Keywords: neuropeptide, periplaneta, RF-amide, perisulfakinin, DUM neuron, Ca2+ channel, TRPγ channel, volume transmission
Copyright: © 2007 Wicher, Derst, Gautier, Lapied, Heinemann and Agricola. This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.
*Correspondence: Dieter Wicher, Department of Evolutionary Neuroethology, Max Planck Institute for Chemical Ecology, Hans-Knöll-Str. 8, D-07745 Jena, Germany. e-mail: dwicher@ice.mpg.de
Citation: Wicher D, Derst C, Gautier H, Lapied B, Heinemann SH and Agricola H (2007) The satiety signaling neuropeptide perisulfakinin inhibits the activity of central neurons promoting general activity. Front. Cell. Neurosci. (2007) 1:3. doi:10.3389/neuro.03.003.2007
Received: 05 September 2007; paper pending published: 12 December 2007; accepted: 13 December 2007; published online: 30 December 2007.
Edited by:
Alexander Borst, Max Planck Institute of Neurobiology, Germany
Reviewed by:
Jane L. Witten, University of Wisconsin-Milwaukee, USA
*Correspondence: Dieter Wicher, Department of Evolutionary Neuroethology, Max Planck Institute for Chemical Ecology, Hans-Knöll-Str. 8, D-07745 Jena, Germany. e-mail: dwicher@ice.mpg.de
