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Peptidergic signaling in the antennal lobe modulates olfaction
Stockholm University, Faculty of Science, Department of Zoology. funktionell morfologi.
Stockholm University, Faculty of Science, Department of Zoology. funktionell morfologi.
2007 (English)In: 20th European Drosophila Research Coference: EDRC 2007, 2007Conference paper, Published paper (Other academic)
Abstract [en]

The dtk gene in Drosophila encodes five different neuropeptides designated Drosophila tachykinins (DTK 1-5) that are expressed in about 100 neurons in the brain. Two tachykinin receptors (DTKR and NKD) have been identified in Drosophila. Specific neurons of the antennal lobe (AL), the primary center for olfactory processing in the Drosophila brain, express DTKs and the receptor DTKR. The DTKs are colocalized with the inhibitory transmitter GABA in many of the local interneurons (LNs) of the AL. We have investigated the roles of DTKs and DTKR in olfactory behavior by interfering with DTK signaling. By employing the Gal4/UAS system we have directed overexpression or knock-down (using RNAi) of peptides or receptor to different neuron types of the AL. Olfactory behavior was tested in a trap-assay based on a choice of odorant or control. We tested flies with DTK deficiency in two different partly overlapping populations of LNs. We also tested flies that are virtually DTK null (driving the RNAi construct with the pan-neural elav-Gal4). DTK deficient flies were less attracted to some of the odors tested. To study the role of the DTKR we used Gal4 lines that drive expression in olfactory receptor neurons (ORNs), LNs and in projection neurons to overexpress (OE) or down-regulate the receptor. DTKR-OE in the ORNs resulted in flies more repelled (or less attracted) to some of the odors tested. DTKR-OE in a subpopulation of the LNs produced flies with the same behavioral phenotype. Flies with DTKR deficiency in the ORNs and LNs were more attracted to odors. Our results suggest that DTKs and DTKR are involved in the modulation of the response to odors at the levels of ORNs and LNs, possibly by modulating the inhibitory activity of GABA.

Place, publisher, year, edition, pages
2007.
National Category
Neurosciences
Identifiers
URN: urn:nbn:se:su:diva-19527OAI: oai:DiVA.org:su-19527DiVA: diva2:186051
Available from: 2007-11-12 Created: 2007-11-12 Last updated: 2009-11-27Bibliographically approved

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