ArticleFrontiers in cellular neuroscience2007
The satiety signaling neuropeptide perisulfakinin inhibits the activity of central neurons promoting general activity.
Article in Frontiers in cellular neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 27 citations in OpenAlex.
- Mass Spectrometry-Based Peptide Profiling of Haemolymph fromMolecules (Basel, Switzerland) · 2022Article
- Analysis of rhodopsin G protein-coupled receptor orthologs reveals semiochemical peptides for parasite (Schistosoma mansoni) and host (Biomphalaria glabrata) interplay.Scientific reports · 2022Article
- Cholecystokinin/sulfakinin peptide signaling: conserved roles at the intersection between feeding, mating and aggression.Cellular and molecular life sciences : CMLS · 2022Review
- Identification and functional characterization of the sulfakinin and sulfakinin receptor in the Chinese white pine beetleFrontiers in physiology · 2022Article
- Sulfakinins influence lipid composition and insulin-like peptides level in oenocytes of Zophobas atratus beetles.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2022Article
- Cholecystokinin-like peptide mediates satiety by inhibiting sugar attraction.PLoS genetics · 2021Article
- Identification of sulfakinin receptors (SKR) in Tenebrio molitor beetle and the influence of sulfakinins on carbohydrates metabolism.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2020Article
- Identification, Functional Characterization, and Pharmacological Analysis of Two Sulfakinin Receptors in the Medically-Important Insect Rhodnius prolixus.Scientific reports · 2019Article
- Genome-wide identification of Drosophila Hb9 targets reveals a pivotal role in directing the transcriptome within eight neuronal lineages, including activation of nitric oxide synthase and Fd59a/Fox-D.Developmental biology · 2014Article
- Cholecystokinin-Like Peptide (DSK) in Drosophila, Not Only for Satiety Signaling.Frontiers in endocrinology · 2014Article
- Signaling properties and pharmacological analysis of two sulfakinin receptors from the red flour beetle, Tribolium castaneum.PloS one · 2014Article
- More than two decades of research on insect neuropeptide GPCRs: an overview.Frontiers in endocrinology · 2012Article
- Insulin-Producing Cells in the Drosophila Brain also Express Satiety-Inducing Cholecystokinin-Like Peptide, Drosulfakinin.Frontiers in endocrinology · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 (EC(50)=11pM) due to reduction of a pacemaker Ca(2+) current through cAMP-inhibited pTRPgamma channels. PSK increased the intracellular cAMP level while decreasing the intracellular Ca(2+) 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 pTRPgamma channel that is activated by AKH under conditions of food shortage.
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